The document discusses the role of phagocytes, specifically macrophages and neutrophils, in the innate immune response against infection. It describes how neutrophils are recruited from the bloodstream to sites of infection through endothelial activation, rolling, arrest, and migration in response to inflammatory signals. It also outlines the mechanisms phagocytes use to kill pathogens, including enzymatic degradation within phagosomes that fuse with lysosomes/granules, and reactive oxygen and nitrogen species produced during respiratory bursts. Phagocytes play a key role in the early innate immune response by removing pathogens, infected cells, and cellular debris.
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PHAGOCYTOSIS- History • Introduction • Phases of phagocytosis :- a) Margination b) Diapedesis c) Chemotaxis d) Opsonization or Attachment e) Engulfment orIngestion f) Secretion or Degranulation g) Killing or Degradation • Applied Aspects • Recent Advances
https://nabeelbeeran.blogspot.com/
PHAGOCYTOSIS- History • Introduction • Phases of phagocytosis :- a) Margination b) Diapedesis c) Chemotaxis d) Opsonization or Attachment e) Engulfment orIngestion f) Secretion or Degranulation g) Killing or Degradation • Applied Aspects • Recent Advances
02.10.09(b): Phagocytic Cells: Mechanisms of Bacterial Injury and Tissue InjuryOpen.Michigan
Slideshow is from the University of Michigan Medical
School's M1 Immunology sequence
View additional course materials on Open.Michigan:
openmi.ch/med-M1Immunology
Immunity :
It is defined as the resistance exhibited by the host against any
foreign antigen including microorganisms.
Plays a major role in prevention of infectious diseases.
Adaptations of mycobacteria for survival in macrophages sameer tiwariSameer Tiwari
Pathogenesis by mycobacteria requires the exploitation of host-cell signalling pathways to enhance the intracellular survival and persistence of the pathogen.
The disruption of these pathways by mycobacteria causes impaired maturation of phagosomes into phagolysosomes, modulates host-cell apoptotic pathways and suppresses the host immune response
02.10.09(b): Phagocytic Cells: Mechanisms of Bacterial Injury and Tissue InjuryOpen.Michigan
Slideshow is from the University of Michigan Medical
School's M1 Immunology sequence
View additional course materials on Open.Michigan:
openmi.ch/med-M1Immunology
Immunity :
It is defined as the resistance exhibited by the host against any
foreign antigen including microorganisms.
Plays a major role in prevention of infectious diseases.
Adaptations of mycobacteria for survival in macrophages sameer tiwariSameer Tiwari
Pathogenesis by mycobacteria requires the exploitation of host-cell signalling pathways to enhance the intracellular survival and persistence of the pathogen.
The disruption of these pathways by mycobacteria causes impaired maturation of phagosomes into phagolysosomes, modulates host-cell apoptotic pathways and suppresses the host immune response
Non-Specific Immune Response, Innate immunity, inherent immunity, Role in overall immunity of individual, Significance, components involve in Non-Specific Immune Response,
What gives carrot & tomato their red color? What is responsible for the yellow color of papaya & mango. This presentation unlocks the secret behind these facts. Enjoy your journey to the colorful world of CAROTENOIDS.
The main effector cells of innate immunity are macrophages, neutrophils, dendritic cells, and natural killer (NK) cells .
Phagocytosis, release of inflammatory mediators, activation of complement system proteins, as well as synthesis of acute phase proteins, cytokines and chemokines are the main mechanisms in innate immunity
Immune system and its functions
The main effector cells of innate immunity are macrophages, neutrophils, dendritic cells, and natural killer (NK) cells .
Phagocytosis begins with adhesion of the phagocyte surface receptors to the pathogen, which then is internalized into vesicles called phagosomes.
Inside the phagocyte, the phagosome fuses to lysosomes, whose contents are released with consequent digestion and pathogen elimination.
Changes in the oxidase’s gene system components present in phagolysosome membrane lead to disability in respiratory burst and generation of reactive oxygen species (ROS).
Phagocytosis begins with adhesion of the phagocyte surface receptors to the pathogen, which then is internalized into vesicles called phagosomes.
Inside the phagocyte, the phagosome fuses to lysosomes, whose contents are released with consequent digestion and pathogen elimination.
Changes in the oxidase’s gene system components present in phagolysosome membrane lead to disability in respiratory burst and generation of reactive oxygen species (ROS).
This slide covers briefly how intracellular and extracellular bacteria elicits an immune response, how bacteria evade from the immune system, what complement system is, opsonization, neutralisation, septic shock, sepsis, superantigens, phagocytosis, interleukins, Toll-like receptors, a list of diseases caused by bacterias and their names etc.
The cells of the immune system arise from a pluripotent Hematopoietic Stem Cells (HSCs) through a process known as haematopoiesis.
Hematopoiesis involves the production, development, differentiation, and maturation of the blood cells (erythrocytes, megakaryocytes and leukocytes) from HSCs.
Differentiation of the HSC will occur along one of two pathways, giving rise to either a common myeloid progenitor or a common lymphoid progenitor cells in the presence of specific cytokines or soluble mediates (growth factor).
Biochemistry of Hair fall, A complete review of hair fall cause, Types, Current methods of treatment, Natural methods of treatment,
for more detail text see :https://iiopinion.blogspot.in/2017/01/hair-fall-scientific-way-of-treatment.html
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
2. Objective of Lecture
Which cells perform phagocytosis
The physiological location of these cells
The function of phagocytes in the resolution of infection
How phagocytes arrive at the site of infection
The mediators involved in this process and their origin
How phagocytes are activated in response to infection
The mediators involved in this process and their origin
The mechanisms these cells use to kill phagocytosed pathogens
The mediators produced by phagocytes that kill pathogens
The differences in functions of the different subsets of phagocytes
3. The role of phagocytes in innate immunity
The earliest of these mechanisms are preformed and therefore are
constantly available to halt infection.
However, by the time complement activation has taken place, further steps
are usually required to prevent the further development of infection by
removing pathogens, infected cells or cellular debris.
These functions cannot be carried out by preformed mediators and therefore
require the assistance of phagocytes.
Individuals with deficiencies in phagocyte function are highly susceptible to
bacterial infections
4. Macrophage/Monocyte Neutrophil
Morphology Large mononuclear cells with
granular cytoplasm
Smaller cells with multi-lobed
nucleus and neutral cytoplasmic
granules
Location Often resident in tissues (remove
routine cell debris)
Blood – requires recruitment to
site of infection
Killing ability Require activation by bacterial
molecules ±IFNg
Activated during recruitment,
then able to kill internalised
bacteria automatically
After killing Migrate to local lymph nodes Die at site by apoptosis (then
taken up by macrophages)
Antigen
presentation
Can present antigen (Class II up-
regulated by IFNg)
Cannot present antigen (don't
normally express Class II)
5. How are Neutrophils recruited to the site of infection?
Neutrophils are the first cells recruited to the
site of an infection and neutrophils carry out
most of the killing at a site of infection.
However, under normal physiological
conditions, neutrophils are not found in
tissues but mainly in the circulation (2-7 X
109/litre of blood).
Neutrophils therefore have to be recruited
from the blood accross the vascular
endothelium into tissue (extravasation).
This occurs at blood vessels close to sites of
inflammation, as a result of production of a
number of proinflammatory signals :
6. How are Neutrophils recruited to the site of infection?
Pro-inflammatory molecules produced in response to
infection/tissue damage include lipid derived
proinflammatory mediators (e.g. prostaglandins (PGs),
leukotrienes (LTs) and platelet activating factor (PAF)) as well as
reactive oxygen and nitrogen species
Plasma enzymes are activated in response tissue damage such as
Plasmin that degrades clots releasing chemotactic and
vasodilating fibrin breakdown products as well as directly
degrading C5 to C5a. Bradykinin is produced via kallekrein and
causes vasodilation and increased vascular permeability.
Activated complement
components are directly
inflammatory (e.g. C5a)
Others (C3a, C4a also
C5a) cause mast cells to
degranulate releasing
histamine, TNF, IL-1,
LTs and PGs
Proinflammatory
cytokines produced by
tissue phagocytes. These
include IL-1, IL-6, IL-8,
IL-12 and TNF
9. Production of inflammatory mediators causes blood vessels to dilate and become leaky and this slows the local blood flow, causes
cells to marginate and fluid to accumulate in tissues. This produces the characteristics of inflammation : tumor, rubor, calor
and dolor and they also cause the endothelium to become activated. Activation of the endothelium is the first step towards
neutrophil extravasation Recruitment of neutrophils can be divided in to 4 processes:
1. Endothelial activation and Rolling: Neutrophils constitutively express ligands and
receptors (e.g. sialylated carbohyrates and L-selectin respectively) which interact with reciprocal
receptors and ligands (e.g. P- and E-selectin and GlyCAM-1 respectively) on endothelial cells.
Blood vessels near sites of inflammation dilate and blood flow reduces, this allows these
interactions to take place and the neutrophils marginate and roll along endothelium in these
areas. Inflammatory mediators (esp. IL-1 and TNF) increase expression of E and P-selectin on
endothelial cells which can then bind mucins (sialyl -Lewisx, PGSL) on the neutrophil and this
allows tethering of marginated cells.
2. Activation: activation of the neutrophil is essential for extravasation. Neutrophils are
activated by complement components (iC3b, C5a), inflammatorylipid mediators (eg. leukotrienes
(LTB4), PAF), cytokines (IL-8; MIP1b) and bacterial products (e.g. N-formylated peptides such
as N-formyl-methionyl-leucylphenylalanine (fMLP)). Once activated neutrophils must gain
access to the infected tissue. They do this using adhesion molecules (selectins, integrins,
intercellular adhesion molecules (ICAMs)).
3. Arrest: activation of neutrophil causes conformational change in integrin (LFA-1), which
allows it to bind to ICAM. Local inflammatory mediators also cause upregulation of integrins
(e.g. LFA-1, Mac-1) on neutrophils which interact with receptors (e.g. ICAM-1, ICAM-2)
upregulated on endothelium. These stronger interactions allow the neutrophil to stop rolling and
cross the endothelium into tissue in a process known as diapedesis
4. Migration: Next, the Neutrophil responds to a group of molecules called chemoattractants
to make its way between the endothelial cells of the blood vessel by a process called diapedesis.
Chemoattractants include complement protein C5a, bacterial products (e.g. fMLP), lipid
mediators (LTB4, PAF) and cytokines (in particular IL-8, also MIP1b). These chemoattractants
also form a chemical gradient in the tissue, and the neutrophil migrates up this gradient (a
process called chemotaxis) in order to find the site of infection. During this process the
neutrophil is activated and ready to kill on its arrival.
10.
Normal tissues harbour low numbers of resident macrophages that are long lived cells (months compared
with neutrophils (6h in circulation, 2-3 days in tissue). They come under a number of tissue specific names
Kupffer cells (liver), Microglia (brain), Histiocytes (skin), Mesangial cells (kidney). These cells are not
activated and would not automatically be able to kill a pathogen – these cells require to undergo
activation in order to get their pathogen killing processes going. This is important, as most of the time
these macrophages are digesting the normal cell debris or dead cells that result from normal wear and tear
in tissues. Classically activated macrophages can be found in 2 activation states:
i. Primed – this happens in response to IFNg, which is produced mainly by T cells. This causes
macrophages to increase the expression of Class II molecules on their surface, and upregulate
phagocytosis and some killing mechanisms. Natural Killer (NK) cells can act as an innate source of IFNg,
allowing macrophage activation to occur in advance of adaptive immune responses (see Figure).
ii. Hyperactivated – this requires the presence of pathogen derived molecules, the best studied is
lipopolysaccharide (LPS), which is abundant on the surface of gram negative bacteria. LPS causes
macrophages to secrete inflammatory mediators such as IL-1, IL-6 and TNF, and also fully upregulate
their killing machinery
However, macrophages can also be alternatively activated through engagement of different cellular
receptors, or mediators of the innate and adaptive immune responses (see Figure 1 from Gordon (2003)
Nat. Rev. Immunol.)
Macrophage numbers in tissues are topped up by migrating monocytes from the blood and approximately
24 hours after infection, large numbers of monocytes are actively recruited from the blood to the site of
infection. IL-1 induces expression of ICAM on endothelial cells which interacts with beta integrins (e.g.
Mac1(CD11b:CD18)) to induce rolling and adhesion. Like Neutrophils, Monocytes follow gradients of
chemokines to the site of infection of which, IL-8 and MCP (monocyte chemoattractant protein) are
particularly active.
11. Once formed, the pathogen-containing phagosome can then fuse with other
cellular compartments containing microbiocidal products.
Neutrophils have 3 main microbiocidal compartments:
Primary granules - contain serine proteases, lysozyme and
phospholipase A2, highly acidic.
Secondary granules - similar to primary, but also include lactoferrin,
elastase and collagenase
Tertiary granules - at leading edge of migrating neurophil and contains
gelatinases capable of degrading basement membranes
Macrophages kill pathogens by fusing phagosomes with lysosomes which
have similar constituents to the neutrophil primary granule.
In addition to these mediators, phagocytes also posess a variety of oxygen
dependent killing mechanisms. Both phagocytes produce a respiratory
burst which produces superoxides and hydrogen peroxide. Neutrophils
contain an enzyme, myeloperoxidase, which can convert superoxide into
hypochlorite (very effective bleach). Macrophages contain an enzyme called
nitric oxide synthase which is activated by IFNg and TNF (or LPS)
treatment which produced nitric oxide, which is very effective at killing.