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CONTENTS
1 Introduction
2 Microbial profiles
3 Gut microbiota and its importance
3.1 Microbial signal with host cell
3.2 Maintenance of gastro intestinal barrier
3.3 Gut brain axis
3.4 Nutrition metabolism
3.5 Gut microbiota and obesity
4 Factors affecting Gut microbiota
5 Conclusions
6 References
1-INTRODUCTION
The human body is host to trillions of microbes. Some of these are useful, and some
are harmful.Some scientists have estimated that there are 10 times more microbial cells in the
body than there are human cells, while others say that the ratio may be closer to 1:1. Recent
scientific advances in genetics mean that humans know a lot more about the microbes in the
body.Many countries have invested a lot in researching the interactions within the human
body’s ecosystem and their relevance to health and disease.
The two terms microbiota and microbiome are often used to mean the same thing and
are used interchangeably. The microbiome is the name given to all of the genes inside these
microbial cells. The human microbiota consists of a wide variety of bacteria, viruses, fungi,
and other single-celled animals that live in the body. Every human being harbors anywhere
between 10 trillion and 100 trillion microbial cells in a symbiotic relationship. This benefits
both the microbes and their hosts, as long as the body is in a healthy state. Estimates vary, but
there could be over 1,000 different species of microorganism making up the human
microbiota. There are plenty of projects trying to decode the human genome by sequencing
all human genes. In a similar way, the microbiome has been subject to intensive efforts to
unravel all its genetic information. It is a good introduction to the range of habitats for
different types of microbe in the body, including the differences between the dry environment
of the forearm and the wet and oily environment of the armpit. The microbes in the body are
so small that they make up only about 2 to 3 percent of the total weight of the human body,
despite outnumbering the cells.
2- MICROBIAL PROFILES
Humans are colonized by many microorganisms, with approximately the same order
of magnitude of non-human cells as human cells. Some microorganisms that colonize
humans are commensal, meaning they co-exist without harming humans; others have
a mutualistic relationship with their human hosts. Conversely, some non-
pathogenic microorganisms can harm human hosts via the metabolites they produce,
like trimethylamine, which the human body converts to trimethylamine N-oxide via FMO3-
mediated oxidation. Certain microorganisms perform tasks that are known to be useful to the
human host, but the role of most of them is not well understood. Those that are expected to be
present, and that under normal circumstances do not cause disease, are sometimes
deemed normal flora or normal microbiota.
All of these together make up various microbiota: communities of microorganisms
present at different sites on or in the human body.The various microbiota make up the human
microbiome: the totality of microorganism communities spread around the human body.
Collections of microorganisms in different areas play a crucial role in helping
maintain our health — though to do so, the numbers of various types of bacteria, fungi, and
other microorganisms have to remain in perfect balance. All our body parts those are exposed
to environment or have an connection with enviorment are sites of harvour for our
microbiota.These include Skin, External ear canal, Respiratory tract, Gastrointestinal tract,
Outer opening of urethra, External genitalia, Vagina, External eye(lids, conjunctiva) etc.
3-GUT MICROBIOTA
The biggest populations of microbes reside in the gut and the assemblage of those
microbes present in the gastrointestinal tract is known as Gut Microbiota. This used to be
called the microflora of the gut.
Although many different types of microbes live inside GI tract, bacteria are the most
studied. There are upto 1000 species of bacteria in the human gut microbiota, and each of
them plays a different role in human body. Most of them are extremely important for host’s
health, while others may cause disease.
IMPORTANCE OF GUT MICROBIOTA
Humans have evolved to live with microbes for millions of years. During this time,
microbes have learned to play very important roles in the human body. In fact, without the
gut microbiome, it would be very difficult to survive.
The gut microbiome begins to affect your body the moment you are born. You are
first exposed to microbes when you pass through your mother’s birth canal. However, new
evidence suggests that babies may come in contact with some microbes while inside the
womb.
As you grow, your gut microbiome begins to diversify, meaning it starts to contain
many different types of microbial species. Higher microbiome diversity is considered good
for your health. Interestingly, the food you eat affects the diversity of your gut bacteria. As
your microbiome grows, it affects your body in a number of ways, including:
 Protection against pathogen: The α-defensins, microbicidal peptides mainly
produced by Paneth cells, are key components of innate immunity. They control
pathogen growth within the intestine and their production can be directly elicited by
both Gram-negative and Gram-positive bacteria, as well as by bacterial metabolites
(e.g., lipopolysaccharide, lipoteichoic acid, lipid A, and muramyl dipeptide).
 Digesting breast milk: Some of the bacteria that first begin to grow inside babies’
intestines are called Bifidobacteria. They digest the healthy sugars in breast milk that
are important for growth.
 Digesting fiber: Certain bacteria digest fiber, producing short chain fatty acids, which
are important for gut health. Fiber may help prevent weight gain, diabetes, heart
disease and the risk of cancer.
 Helping control your immune system: The gut microbiome also controls how your
immune system works. By communicating with immune cells, the gut microbiome can
control how your body responds to infection.
 Promotion of fat storage: The microbiota promotes storage of Triglycerides in
adipocytes through suppression of intestinal expression of a circulating LPL inhibitor
and absorption of monosaccharides from the gut lumen, with resulting induction of de
novo hepatic lipogenesis.
 Helping control brain health: New research suggests that the gut microbiome may
also affect the central nervous system, which controls brain function.

Fig: Functions of Human Gut Microbiota
Therefore, there are a number of different ways in which the gut microbiota can affect
key bodily functions and influence your health.
3.1- MICROBIAL SIGNAL WITH HOST CELL
Microorganism or cell for their growth, development, sustainability are needed to
communicate with host cells for co-ordination, which is essential for their functionality.
Resident microbiota within the intestinal lumen signal to Enteroendocrine(EE) cells via
multiple pathways.
 Firstly, microbiota convert indigestible carbohydrates to SCF acids, which in turn
signal to EE cells via free fatty acid receptors(FFAR 2/3) or by activation of nuclear
histone deacetylase(HDAC).
 Secondly, microbiota convert primary bile acids to secondary bile acids such as
deoxycholate, which then signal to EE cells via the membrane G protein coupled bile
acid receptor TGR5 or nuclear FARNASOID X receptor(FXR).
 Finally, structural components of microbiota such as flagella and the endotoxin
lipopolysaccharide(LPS) signal to Toll Like Receptors(TLR).
Fig. Microbial Signalling
3.2- MAINTENANCE OF GASTROINTESTINAL BARRIER
Gastrointestinal barrier is important for maintaining gut homeostasis. Mechanisms of
action of the intestinal microbiome on the gastrointestinal barrier. Commensal bacteria
support the digestion of fibres and other nutrients, thereby contributing to energy and
substrate supply.
They regulate epithelial functions such as mucus production in goblet cells, defensin
release from Paneth cells and tight junction protein synthesis in normal epithelial cells. They
prevent colonisation of pathogens in the gut and regulate the mucosal immune system, for
example, by inducing and maintaining gut-associated lymphoid tissue and by stimulating
mucosal immunoglobulin A production. For details and references, see text 'Underlying
mechanisms'.
Fig: Maintenance of gastrointestinal barrier by gut microbiota
3.3- GUT BRAIN AXIS
In general the brain–gut–enteric microbiota axis includes the CNS, the
neuroendocrine and neuroimmune systems, the sympathetic and parasympathetic arms of the
autonomic nervous system (ANS), the enteric nervous system (ENS), and of course the
intestinal microbiota. During the feeding, the gut released peptides which are affecting
hypothalamic pathways, and especially arcuate nucleus involved in the regulation of satiety
and metabolism. Through this bidirectional communication network, signals from the brain
can influence the motor, sensory, and secretory modalities of the GIT and conversely,
visceral messages from the GIT can influence brain function.
The vagus nerve is the direct communication observed between the bacteria and the
brain. The cross talk between gut microbiota, the immune system and the brain-gut axis plays
an important role in the modulation of the stress response of the gut in the context of the
development of different gut disorders as microbiota communicate with the gut-brain axis
through different mechanisms viz. direct interaction with mucosal cells (endocrine message),
via immune cells (immune message), and via contact to neural endings.
Fig: Microbiota-Gut-Brain Axis
Microbiota also interacts with host gut-brain axis through neurohumoral
communication to influence brain development and behavior. For example, alteration in
gastrointestinal function is communicated to the brain bringing about the perception of
visceral events such as nausea, satiety, and pain or when, in turn, stressful experiences lead to
altered gastrointestinal secretions and motility.
The neuroendocrine, neuroimmune, the sympathetic and parasympathetic arms of the
autonomic nervous system and the enteric nervous system are the key pathways through
which they communicate with each other. This might influence a broad spectrum of diseases,
psychiatric conditions and other disorders.microbes access the brain and influence behavior
include microbial products that gain access to the brain, via cytokine release from the
mucosal immune cells, via the release of gut hormones such as 5-HT from endocrine cells, or
via afferent neural pathways, including the vagus nerve.
Stress and emotions can also influence the microbial composition of the gut through
the release of stress hormones or sympathetic neurotransmitters (GABA, 5-HT precursors
etc.) that influence gut physiology and alter the habitat of the microbiota and also these
catecholamine alter the growth, motility and virulence of pathogenic and commensally
bacteria. Alternatively, host stress hormones such as noradrenalin might influence bacterial
gene expression or signaling between bacteria, and this might change the microbial
composition and activity of the microbiota.
3.4-NUTRITION METABOLISM
Fig: The influence of Gut microbiota on host metabolism
 The gut microbiota provides essential capacities for the fermentation of non-digestible
substrates like dietary fibres and endogenous intestinal mucus. This fermentation
supports the growth of specialist microbes that produce short chain fatty acids
(SCFAs) and gases. The major SCFAs produced are acetate, propionate, and butyrate.
 Butyrate is the main energy source for human colonocytes, can induce apoptosis of
colon cancer cells, and can activate intestinal gluconeogenesis, having beneficial
effects on glucose and energy homeostasis.Butyrate is essential for epithelial cells to
consume large amounts of oxygen through β oxidation, generating a state of hypoxia
that maintains oxygen balance in the gut, preventing gut microbiota dysbiosis.
 Propionate is transferred to the liver, where it regulates gluconeogenesis and satiety
signalling through interaction with the gut fatty acid receptors 1. Acetate—the most
abundant SCFA and an essential metabolite for the growth of other bacteria—reaches
the peripheral tissues where it is used in cholesterol metabolism and lipogenesis, and
may play a role in central appetite regulation. Randomised controlled trials have
shown that higher production of SCFAs correlates with lower diet-induced
obesity and with reduced insulin resistance.
 Gut microbial enzymes contribute to bile acid metabolism, generating unconjugated
and secondary bile acids that act as signalling molecules and metabolic regulators to
influence important host pathways.
 Other specific products of the gut microbiota have been implicated directly in human
health outcomes. Examples include trimethylamine and indolepropionic acid. The
production of trimethylamine from dietary phosphatidylcholine and carnitine (from
meat and dairy) depends on the gut microbiota and thus its amount in blood varies
between people.
 Trimethylamine is oxidised in the liver to trimethylamine N-oxide, which is positively
associated with an increased risk of atherosclerosis and major adverse cardiovascular
events. Indolepropionic acid is highly correlated with dietary fibre intake and has
potent radical scavenging activity in vitro, which seems to reduce the risk of incidence
of type 2 diabetes.
3.5-THE GUT MICROBIOTA AND OBESITY
The gut microbiota seems to play a role in the development and progression of
obesity. Most studies of overweight and obese people show a dysbiosis characterised by a
lower diversity. Germ-free mice that receive faecal microbes from obese humans gain more
weight than mice that receive microbes from healthy weight humans. A large study of UK
twins found that the genus Christensenella was rare in overweight people and when given to
germ free mice prevented weight gain. This microbe and others such
as Akkermansia correlate with lower visceral fat deposits.Although much of the confirmatory
evidence comes from mouse models, long term weight gain (over 10 years) in humans
correlates with low microbiota diversity, and this association is exacerbated by low dietary
fibre intake.
Acquisition of the intestinal microbiota begins at birth, and a stable microbial
community develops from a succession of key organisms. Disruption of the microbiota
during maturation by low-dose antibiotic exposure can alter host metabolism and adiposity.
Low-dose penicillin (LDP), delivered from birth, induces metabolic alterations and affects
ileal expression of genes involved in immunity. LDP that is limited to early life transiently
perturbs the microbiota, which is sufficient to induce sustained effects on body composition,
indicating that microbiota interactions in infancy may be critical determinants of long-term
host metabolic effects. In addition, LDP enhances the effect of high-fat diet induced obesity.
The growth promotion phenotype is transferrable to germ-free hosts by LDP-selected
microbiota, showing that the altered microbiota..
 Early life is a critical window of host-microbe metabolic interaction
 Low-dose penicillin treatment amplifies diet-induced obesity
 A transient early microbiota perturbation leads to long-term increased adiposity
 The penicillin-altered microbiota has a causal role in inducing metabolic changes
Fig: Connection between gut microbiota and obesity in Mouse
4- FACTORS AFFECTING GUT MICROBIOTA
Diet :-
The type of food that a person consumes can have a significant impact on gut
microbiota.The western diet, which is high in fat and low in fiber, is linked to a decrease in
overall total bacteria and beneficial Bifidobacterium and Eubacterium species. This alteration
can lead to mucus degradation, reduced levels of short-chain fatty acids, and increased
susceptibility to invading pathogens. Bifidobacterium and Eubacterium species and overall
total bacteria count are increased with high-fiber diets, such as the Mediterranean diet.
Pharmaceuticals :-
Certain medications, such as antibiotics and proton pump inhibitors, can alter gut
microbial composition. Proton pump inhibitors reduce acidity in the GI tract, creating a
higher luminal pH, which can promote small intestinal bacterial overgrowth. Antibiotic use
can diminish taxonomic diversity, which can persist over time.
Physical activity :-
Habitual exercise is associated with increased diversity and abundance of gut
microbiota and boosts production of beneficial short-chain fatty acids.
Psychological stress/anxiety :-
Psychological stress can affect gut motility, visceral perception, GI secretion, and
intestinal permeability. These effects on the GI tract can negativity alter the composition of
gut microbiota.
Infection :-
Infection is one of the most common causes of dysbiosis. Colonization by pathogenic bacteria
can induce inflammation in the GI tract. This inflammatory state can destabilize the gut
microbiota community, resulting in an imbalance in composition and function. In addition,
pathogens can outcompete commensal bacteria, resulting in overgrowth of infectious
bacteria.
Age :-
Microbial diversity increases in early childhood and stabilizes at age 3. After age 70 immune
system weakens and changes in physical activity, digestion and nutrient intake can affect
microbial composition. The resulting dysbiosis can trigger proinflammatory state that may be
linked to health issues, such as malnutrition and tumorgenesis.
Dysbiosis :-
Current research supports that gut microbiota ,in some capacity ,contribute not only to
the maintenance of GI health but also to the development of many GI diseases
GI conditions linked to Gut microbial imbalance;-
 Irritable bowel syndrome
 Inflammatory bowel disease
 Chronic liver disease
 Peptic ulcer disease
 Clostridium difficile colitis
 Celiac disease
Fig: Factors affecting Gut Microbiota
CONCLUSIONS :-
 The indigenous gastrointestinal tract microflora has profound effects on the
anatomical, physiological and immunological development of the host.
 Large-scale efforts have described in great detail the constituents of the healthy
human microbiota and its functional capacity, and these studies are followed by
similar characterizations of the microbiota in particular diseased states.
 These studies will provide further insight into the host microbiota interactions that
contribute to healthy and disease, and eventually lead to therapies targeting the
microbiota to maintain healthy and to treat a variety of diseases.
6-REFERENCES :-
 The Gut Microbiome and its Effects on Human Health By Bassel A.
 What are the gut microbiota and human microbiome? By Markus MacGill
 https://www.researchgate.net/figure/The-intestines-impact-on-health-The-
gastrointestinal-tract-contributes-to-health-by_fig1_50394128
 The influence of The Gut Microbiome on Host Metabolism Through the Regulation
of Gut Hormone Release By Alyce M. Martin, Emily W. Sun
Acknowledgement
I am highly indebted to express my obligation to Dr. Puspanjali Parida, Department of
Zoology, Maharaja Sriram Chandra Bhanjadeo University, Takatpur, Baripada, Odisha for
her proper & valuable guidance, suggestion and solving the problem, supervision and
constant encouragement in the preparation of the seminar report successfully.
I would like to express my gratitude to all the faculty members including Dr.
Puspanjali Parida, Dr. Priyaranjan Debata, Dr. Cuckoo Mahapatra, Dr.Gargee Mohanty for
their kind help and support in the progress of the seminar report. I express my thanks to all
the friends, my juniors and seniors for their inspiriting words, co-operation and their
encouragement.
Sonali Das
Certificate
This is to certify that Sonali Das, of the Department of Zoology, Maharaja
Sriram Chandra Bhanjadeo University, Takatpur, Baripada has satisfactorily
completed the seminar report on “The Gut Microbiota and Its Role On Human
Health” under my guidance delivered by him and submitted to the P.G. Department of
Zoology, Maharaja Sriram Chandra Bhanjadeo University, Takatpur, Baripada for the
session 2021-22.
Dr. Hemanta Kumar Sahu
A
SEMINAR REPORT ON
“THE GUT MICROBIOTA & ITS ROLE ON
HUMAN HEALTH”
Submitted by Sonali Das
2 nd Semester
Roll no- 13001N202004
Redg. No- 02222/20
Guided By
Dr. Puspanjali Parida
POST- GRADUATE DEPARTMENT OF ZOOLOGY
MAHARAJA SRIRAM CHANDRA BHANJDEO UNIVERSITY,
TAKATPUR BARIPADA, ODISHA, 757003

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presentation write up (1).pdf

  • 1. CONTENTS 1 Introduction 2 Microbial profiles 3 Gut microbiota and its importance 3.1 Microbial signal with host cell 3.2 Maintenance of gastro intestinal barrier 3.3 Gut brain axis 3.4 Nutrition metabolism 3.5 Gut microbiota and obesity 4 Factors affecting Gut microbiota 5 Conclusions 6 References
  • 2. 1-INTRODUCTION The human body is host to trillions of microbes. Some of these are useful, and some are harmful.Some scientists have estimated that there are 10 times more microbial cells in the body than there are human cells, while others say that the ratio may be closer to 1:1. Recent scientific advances in genetics mean that humans know a lot more about the microbes in the body.Many countries have invested a lot in researching the interactions within the human body’s ecosystem and their relevance to health and disease. The two terms microbiota and microbiome are often used to mean the same thing and are used interchangeably. The microbiome is the name given to all of the genes inside these microbial cells. The human microbiota consists of a wide variety of bacteria, viruses, fungi, and other single-celled animals that live in the body. Every human being harbors anywhere between 10 trillion and 100 trillion microbial cells in a symbiotic relationship. This benefits both the microbes and their hosts, as long as the body is in a healthy state. Estimates vary, but there could be over 1,000 different species of microorganism making up the human microbiota. There are plenty of projects trying to decode the human genome by sequencing all human genes. In a similar way, the microbiome has been subject to intensive efforts to unravel all its genetic information. It is a good introduction to the range of habitats for different types of microbe in the body, including the differences between the dry environment of the forearm and the wet and oily environment of the armpit. The microbes in the body are so small that they make up only about 2 to 3 percent of the total weight of the human body, despite outnumbering the cells. 2- MICROBIAL PROFILES Humans are colonized by many microorganisms, with approximately the same order of magnitude of non-human cells as human cells. Some microorganisms that colonize humans are commensal, meaning they co-exist without harming humans; others have a mutualistic relationship with their human hosts. Conversely, some non- pathogenic microorganisms can harm human hosts via the metabolites they produce, like trimethylamine, which the human body converts to trimethylamine N-oxide via FMO3- mediated oxidation. Certain microorganisms perform tasks that are known to be useful to the
  • 3. human host, but the role of most of them is not well understood. Those that are expected to be present, and that under normal circumstances do not cause disease, are sometimes deemed normal flora or normal microbiota. All of these together make up various microbiota: communities of microorganisms present at different sites on or in the human body.The various microbiota make up the human microbiome: the totality of microorganism communities spread around the human body. Collections of microorganisms in different areas play a crucial role in helping maintain our health — though to do so, the numbers of various types of bacteria, fungi, and other microorganisms have to remain in perfect balance. All our body parts those are exposed to environment or have an connection with enviorment are sites of harvour for our microbiota.These include Skin, External ear canal, Respiratory tract, Gastrointestinal tract, Outer opening of urethra, External genitalia, Vagina, External eye(lids, conjunctiva) etc.
  • 4. 3-GUT MICROBIOTA The biggest populations of microbes reside in the gut and the assemblage of those microbes present in the gastrointestinal tract is known as Gut Microbiota. This used to be called the microflora of the gut. Although many different types of microbes live inside GI tract, bacteria are the most studied. There are upto 1000 species of bacteria in the human gut microbiota, and each of them plays a different role in human body. Most of them are extremely important for host’s health, while others may cause disease. IMPORTANCE OF GUT MICROBIOTA Humans have evolved to live with microbes for millions of years. During this time, microbes have learned to play very important roles in the human body. In fact, without the gut microbiome, it would be very difficult to survive.
  • 5. The gut microbiome begins to affect your body the moment you are born. You are first exposed to microbes when you pass through your mother’s birth canal. However, new evidence suggests that babies may come in contact with some microbes while inside the womb. As you grow, your gut microbiome begins to diversify, meaning it starts to contain many different types of microbial species. Higher microbiome diversity is considered good for your health. Interestingly, the food you eat affects the diversity of your gut bacteria. As your microbiome grows, it affects your body in a number of ways, including:  Protection against pathogen: The α-defensins, microbicidal peptides mainly produced by Paneth cells, are key components of innate immunity. They control pathogen growth within the intestine and their production can be directly elicited by both Gram-negative and Gram-positive bacteria, as well as by bacterial metabolites (e.g., lipopolysaccharide, lipoteichoic acid, lipid A, and muramyl dipeptide).  Digesting breast milk: Some of the bacteria that first begin to grow inside babies’ intestines are called Bifidobacteria. They digest the healthy sugars in breast milk that are important for growth.  Digesting fiber: Certain bacteria digest fiber, producing short chain fatty acids, which are important for gut health. Fiber may help prevent weight gain, diabetes, heart disease and the risk of cancer.  Helping control your immune system: The gut microbiome also controls how your immune system works. By communicating with immune cells, the gut microbiome can control how your body responds to infection.  Promotion of fat storage: The microbiota promotes storage of Triglycerides in adipocytes through suppression of intestinal expression of a circulating LPL inhibitor and absorption of monosaccharides from the gut lumen, with resulting induction of de novo hepatic lipogenesis.  Helping control brain health: New research suggests that the gut microbiome may also affect the central nervous system, which controls brain function.
  • 6.  Fig: Functions of Human Gut Microbiota Therefore, there are a number of different ways in which the gut microbiota can affect key bodily functions and influence your health. 3.1- MICROBIAL SIGNAL WITH HOST CELL Microorganism or cell for their growth, development, sustainability are needed to communicate with host cells for co-ordination, which is essential for their functionality. Resident microbiota within the intestinal lumen signal to Enteroendocrine(EE) cells via multiple pathways.  Firstly, microbiota convert indigestible carbohydrates to SCF acids, which in turn signal to EE cells via free fatty acid receptors(FFAR 2/3) or by activation of nuclear histone deacetylase(HDAC).  Secondly, microbiota convert primary bile acids to secondary bile acids such as deoxycholate, which then signal to EE cells via the membrane G protein coupled bile acid receptor TGR5 or nuclear FARNASOID X receptor(FXR).  Finally, structural components of microbiota such as flagella and the endotoxin lipopolysaccharide(LPS) signal to Toll Like Receptors(TLR).
  • 7. Fig. Microbial Signalling 3.2- MAINTENANCE OF GASTROINTESTINAL BARRIER Gastrointestinal barrier is important for maintaining gut homeostasis. Mechanisms of action of the intestinal microbiome on the gastrointestinal barrier. Commensal bacteria support the digestion of fibres and other nutrients, thereby contributing to energy and substrate supply. They regulate epithelial functions such as mucus production in goblet cells, defensin release from Paneth cells and tight junction protein synthesis in normal epithelial cells. They prevent colonisation of pathogens in the gut and regulate the mucosal immune system, for example, by inducing and maintaining gut-associated lymphoid tissue and by stimulating mucosal immunoglobulin A production. For details and references, see text 'Underlying mechanisms'.
  • 8. Fig: Maintenance of gastrointestinal barrier by gut microbiota 3.3- GUT BRAIN AXIS In general the brain–gut–enteric microbiota axis includes the CNS, the neuroendocrine and neuroimmune systems, the sympathetic and parasympathetic arms of the autonomic nervous system (ANS), the enteric nervous system (ENS), and of course the intestinal microbiota. During the feeding, the gut released peptides which are affecting hypothalamic pathways, and especially arcuate nucleus involved in the regulation of satiety and metabolism. Through this bidirectional communication network, signals from the brain can influence the motor, sensory, and secretory modalities of the GIT and conversely, visceral messages from the GIT can influence brain function. The vagus nerve is the direct communication observed between the bacteria and the brain. The cross talk between gut microbiota, the immune system and the brain-gut axis plays an important role in the modulation of the stress response of the gut in the context of the development of different gut disorders as microbiota communicate with the gut-brain axis through different mechanisms viz. direct interaction with mucosal cells (endocrine message), via immune cells (immune message), and via contact to neural endings.
  • 9. Fig: Microbiota-Gut-Brain Axis Microbiota also interacts with host gut-brain axis through neurohumoral communication to influence brain development and behavior. For example, alteration in gastrointestinal function is communicated to the brain bringing about the perception of visceral events such as nausea, satiety, and pain or when, in turn, stressful experiences lead to altered gastrointestinal secretions and motility. The neuroendocrine, neuroimmune, the sympathetic and parasympathetic arms of the autonomic nervous system and the enteric nervous system are the key pathways through which they communicate with each other. This might influence a broad spectrum of diseases, psychiatric conditions and other disorders.microbes access the brain and influence behavior include microbial products that gain access to the brain, via cytokine release from the mucosal immune cells, via the release of gut hormones such as 5-HT from endocrine cells, or via afferent neural pathways, including the vagus nerve. Stress and emotions can also influence the microbial composition of the gut through the release of stress hormones or sympathetic neurotransmitters (GABA, 5-HT precursors etc.) that influence gut physiology and alter the habitat of the microbiota and also these
  • 10. catecholamine alter the growth, motility and virulence of pathogenic and commensally bacteria. Alternatively, host stress hormones such as noradrenalin might influence bacterial gene expression or signaling between bacteria, and this might change the microbial composition and activity of the microbiota. 3.4-NUTRITION METABOLISM Fig: The influence of Gut microbiota on host metabolism  The gut microbiota provides essential capacities for the fermentation of non-digestible substrates like dietary fibres and endogenous intestinal mucus. This fermentation supports the growth of specialist microbes that produce short chain fatty acids (SCFAs) and gases. The major SCFAs produced are acetate, propionate, and butyrate.  Butyrate is the main energy source for human colonocytes, can induce apoptosis of colon cancer cells, and can activate intestinal gluconeogenesis, having beneficial effects on glucose and energy homeostasis.Butyrate is essential for epithelial cells to consume large amounts of oxygen through β oxidation, generating a state of hypoxia that maintains oxygen balance in the gut, preventing gut microbiota dysbiosis.
  • 11.  Propionate is transferred to the liver, where it regulates gluconeogenesis and satiety signalling through interaction with the gut fatty acid receptors 1. Acetate—the most abundant SCFA and an essential metabolite for the growth of other bacteria—reaches the peripheral tissues where it is used in cholesterol metabolism and lipogenesis, and may play a role in central appetite regulation. Randomised controlled trials have shown that higher production of SCFAs correlates with lower diet-induced obesity and with reduced insulin resistance.  Gut microbial enzymes contribute to bile acid metabolism, generating unconjugated and secondary bile acids that act as signalling molecules and metabolic regulators to influence important host pathways.  Other specific products of the gut microbiota have been implicated directly in human health outcomes. Examples include trimethylamine and indolepropionic acid. The production of trimethylamine from dietary phosphatidylcholine and carnitine (from meat and dairy) depends on the gut microbiota and thus its amount in blood varies between people.  Trimethylamine is oxidised in the liver to trimethylamine N-oxide, which is positively associated with an increased risk of atherosclerosis and major adverse cardiovascular events. Indolepropionic acid is highly correlated with dietary fibre intake and has potent radical scavenging activity in vitro, which seems to reduce the risk of incidence of type 2 diabetes. 3.5-THE GUT MICROBIOTA AND OBESITY The gut microbiota seems to play a role in the development and progression of obesity. Most studies of overweight and obese people show a dysbiosis characterised by a lower diversity. Germ-free mice that receive faecal microbes from obese humans gain more weight than mice that receive microbes from healthy weight humans. A large study of UK twins found that the genus Christensenella was rare in overweight people and when given to germ free mice prevented weight gain. This microbe and others such as Akkermansia correlate with lower visceral fat deposits.Although much of the confirmatory evidence comes from mouse models, long term weight gain (over 10 years) in humans
  • 12. correlates with low microbiota diversity, and this association is exacerbated by low dietary fibre intake. Acquisition of the intestinal microbiota begins at birth, and a stable microbial community develops from a succession of key organisms. Disruption of the microbiota during maturation by low-dose antibiotic exposure can alter host metabolism and adiposity. Low-dose penicillin (LDP), delivered from birth, induces metabolic alterations and affects ileal expression of genes involved in immunity. LDP that is limited to early life transiently perturbs the microbiota, which is sufficient to induce sustained effects on body composition, indicating that microbiota interactions in infancy may be critical determinants of long-term host metabolic effects. In addition, LDP enhances the effect of high-fat diet induced obesity. The growth promotion phenotype is transferrable to germ-free hosts by LDP-selected microbiota, showing that the altered microbiota..  Early life is a critical window of host-microbe metabolic interaction  Low-dose penicillin treatment amplifies diet-induced obesity  A transient early microbiota perturbation leads to long-term increased adiposity  The penicillin-altered microbiota has a causal role in inducing metabolic changes Fig: Connection between gut microbiota and obesity in Mouse
  • 13. 4- FACTORS AFFECTING GUT MICROBIOTA Diet :- The type of food that a person consumes can have a significant impact on gut microbiota.The western diet, which is high in fat and low in fiber, is linked to a decrease in overall total bacteria and beneficial Bifidobacterium and Eubacterium species. This alteration can lead to mucus degradation, reduced levels of short-chain fatty acids, and increased susceptibility to invading pathogens. Bifidobacterium and Eubacterium species and overall total bacteria count are increased with high-fiber diets, such as the Mediterranean diet. Pharmaceuticals :- Certain medications, such as antibiotics and proton pump inhibitors, can alter gut microbial composition. Proton pump inhibitors reduce acidity in the GI tract, creating a higher luminal pH, which can promote small intestinal bacterial overgrowth. Antibiotic use can diminish taxonomic diversity, which can persist over time. Physical activity :- Habitual exercise is associated with increased diversity and abundance of gut microbiota and boosts production of beneficial short-chain fatty acids. Psychological stress/anxiety :- Psychological stress can affect gut motility, visceral perception, GI secretion, and intestinal permeability. These effects on the GI tract can negativity alter the composition of gut microbiota. Infection :- Infection is one of the most common causes of dysbiosis. Colonization by pathogenic bacteria can induce inflammation in the GI tract. This inflammatory state can destabilize the gut microbiota community, resulting in an imbalance in composition and function. In addition, pathogens can outcompete commensal bacteria, resulting in overgrowth of infectious bacteria.
  • 14. Age :- Microbial diversity increases in early childhood and stabilizes at age 3. After age 70 immune system weakens and changes in physical activity, digestion and nutrient intake can affect microbial composition. The resulting dysbiosis can trigger proinflammatory state that may be linked to health issues, such as malnutrition and tumorgenesis. Dysbiosis :- Current research supports that gut microbiota ,in some capacity ,contribute not only to the maintenance of GI health but also to the development of many GI diseases GI conditions linked to Gut microbial imbalance;-  Irritable bowel syndrome  Inflammatory bowel disease  Chronic liver disease  Peptic ulcer disease  Clostridium difficile colitis  Celiac disease Fig: Factors affecting Gut Microbiota
  • 15. CONCLUSIONS :-  The indigenous gastrointestinal tract microflora has profound effects on the anatomical, physiological and immunological development of the host.  Large-scale efforts have described in great detail the constituents of the healthy human microbiota and its functional capacity, and these studies are followed by similar characterizations of the microbiota in particular diseased states.  These studies will provide further insight into the host microbiota interactions that contribute to healthy and disease, and eventually lead to therapies targeting the microbiota to maintain healthy and to treat a variety of diseases. 6-REFERENCES :-  The Gut Microbiome and its Effects on Human Health By Bassel A.  What are the gut microbiota and human microbiome? By Markus MacGill  https://www.researchgate.net/figure/The-intestines-impact-on-health-The- gastrointestinal-tract-contributes-to-health-by_fig1_50394128  The influence of The Gut Microbiome on Host Metabolism Through the Regulation of Gut Hormone Release By Alyce M. Martin, Emily W. Sun
  • 16. Acknowledgement I am highly indebted to express my obligation to Dr. Puspanjali Parida, Department of Zoology, Maharaja Sriram Chandra Bhanjadeo University, Takatpur, Baripada, Odisha for her proper & valuable guidance, suggestion and solving the problem, supervision and constant encouragement in the preparation of the seminar report successfully. I would like to express my gratitude to all the faculty members including Dr. Puspanjali Parida, Dr. Priyaranjan Debata, Dr. Cuckoo Mahapatra, Dr.Gargee Mohanty for their kind help and support in the progress of the seminar report. I express my thanks to all the friends, my juniors and seniors for their inspiriting words, co-operation and their encouragement. Sonali Das
  • 17. Certificate This is to certify that Sonali Das, of the Department of Zoology, Maharaja Sriram Chandra Bhanjadeo University, Takatpur, Baripada has satisfactorily completed the seminar report on “The Gut Microbiota and Its Role On Human Health” under my guidance delivered by him and submitted to the P.G. Department of Zoology, Maharaja Sriram Chandra Bhanjadeo University, Takatpur, Baripada for the session 2021-22. Dr. Hemanta Kumar Sahu
  • 18. A SEMINAR REPORT ON “THE GUT MICROBIOTA & ITS ROLE ON HUMAN HEALTH” Submitted by Sonali Das 2 nd Semester Roll no- 13001N202004 Redg. No- 02222/20 Guided By Dr. Puspanjali Parida POST- GRADUATE DEPARTMENT OF ZOOLOGY MAHARAJA SRIRAM CHANDRA BHANJDEO UNIVERSITY, TAKATPUR BARIPADA, ODISHA, 757003