This document provides an overview of inflammatory bowel disease (IBD), including ulcerative colitis and Crohn's disease. IBD is a chronic inflammatory condition of the gastrointestinal tract caused by genetic and environmental factors that lead to an abnormal immune response. The two main types are ulcerative colitis, which affects only the colon, and Crohn's disease, which can impact any part of the GI tract. Symptoms vary depending on the specific type and location of inflammation. Treatment aims to reduce inflammation, manage complications, and maintain remission through nutritional support, medications like immunosuppressants, and potentially surgery in severe cases.

1. AMITY INSTITUTE OF BIOTECHNOLOGY
AN ASSIGNMENT ON
“INFLAMMATORY BOWEL DISEASE(IBD)”
SUBMITTED BY:
SAMIM KHAN
M.Sc.(BT) 3rd
sem.
A7100216002

2. INTRODUTION:-
Inflammatory bowel disease (IBD), comprising Crohn’s disease (CD) and ulcerative
colitis (UC), is a chronic, relapsing-remitting inflammatory disorder of the gastrointestinal (GI)
tract. CD and UC vary in the region of the GI tract they affect; the extent of inflammation and
resulting tissue damage; and their associated symptoms. UC tends to exhibit continuous
superficial inflammation which spreads from the rectum and is limited to the colon (large
intestine), with bloody diarrhoea as the most common symptom. Inflammation associated with
CD is transmural (affects all layers of GI tract tissue), patchy (areas of inflammation are
interspersed with healthy unaffected tissue) and can present anywhere along the entire GI tract
and, in some cases, in the skin and joints. The symptoms of CD are more diverse than for UC,
including diarrhoea, abdominal pain and weight loss.
The exact cause of IBD is unclear. There appear to be four main factors which influence the
disease: host genetic susceptibility, a dysregulated immune response and impairment of intestinal
epithelial barrier function, and environmental factors
Factors internal and external to the host that influence inflammatory bowel disease (IBD)

3. Genetic susceptibility:-
Genome-wide association studies (GWASs) have identified a number of genetic loci associated
with IBD, including genes specific to either CD or UC, and some which are common to both.
The risk of developing IBD conferred by variants at each locus is small for all but a few genes
(e.g. IL10RA and IL10RB). It may be the case that IBD only occurs when multiple genetic
variations associated with the disease are present. Another possibility is that environmental
factors are required to trigger the onset of disease in genetically susceptible individuals.
Environmental factors:-
Environmental factors such as the commensal microflora, pathogenic infections and metabolic
factors are thought to play a role in the development and perpetuation of IBD. The intestinal
microbiota, which is dominated by bacteria, but also includes viruses, fungi and protozoa, is
crucial for development of the host immune system but also appears to be the target of the
inflammatory response during IBD. The composition of the intestinal microbiota appears to be
altered during disease, although whether this causes, or results from, intestinal inflammation is
unclear. The effects of antibiotics, pathogenic infections and diet on IBD might be explained by
their impact on the commensal microflora.
TYPE:-
Two major types of IBD are
 ulcerative colitis :- Ulcerative colitis is limited to the colon or large intestine.
 Crohn's disease:- Crohn's disease, on the other hand, can involve any part of the
gastrointestinal tract from the mouthto the anus. Most commonly, though, it affects
the last part of the small intestine or the colon or both.

4. MECHANISM:-
It is thought that IBD develops because of an abnormal host response to an environmental trigger
in genetically susceptible individuals. This causes inflammation of the intestine and release of
inflammatory mediators, such as TNF, IL-12 and IL-23, which cause tissue damage. These
mediators are targets for therapeutic intervention. In both diseases the intestinal wall is infiltrated
with acute and chronic inflammatory cells.
There are important differences in the distribution of disease and in histological features
(1) Bacterial antigens are taken up by specialised M cells, pass between leaky epithelial cells
or enter the lamina propria through ulcerated mucosa.
(2) After processing they are presented to type 1 T-helper cells by antigen-presenting cells
(APC) in the lamina propria.
(3) T-cell activation and differentiation results in a Th1 T cell-mediated cytokine response
(4) with secretion of cytokines including gamma interferon (IFN-γ). Further amplification of
T cells perpetuates the inflammatory process with activation of non-immune cells and
release of other important cytokines, e.g. (IL)-12, IL-23, IL-1, IL-6 and tumour necrosis
factor (TNF).
These pathways occur in all normal individuals exposed to an inflammatory insult and this is
self-limiting in healthy subjects. In genetically predisposed persons, dysregulation of innate
immunity may trigger inflammatory bowel disease.
Immune Mechanism of Inflammatory Bowel Disease

5. Signs and symptoms:-
 Malaise and fever
 Abdominal pain
 Frequent bowel movements
 Hematochezia
 Fistula
 Weight loss
 Arthritis
Treatment:
DESIRED OUTCOME
To treat IBD properly, the clinician must have a clear concept of realistic therapeutic goals for
each patient.
These goals may relate to
 Resolution of acute inflammatory processes
 Resolution of attendant complications (e.g., fistulas and abscesses), Alleviation of
systemic manifestations (e.g., arthritis),
 Maintenance of remission from acute inflammation, or surgical palliation or cure.
Nutritional Support :
 Many specific diets have been tried to improve the condition of patients with IBD, but
none has gained widespread acceptance.
 With each individual it is helpful to eliminate specific foods that exacerbate symptoms.
 Some patients with IBD, although not the majority, have lactase deficiency;
consequently, diarrhea may be associated with milk intake.
 In such patient avoidance of milk or supplementation with lactase generally improves the
patient’s symptoms.
PHARMACOLOGIC THERAPY :
 Drug therapy plays an integral part in the overall treatment of IBD.
 None of the drugs used for IBD are curative; at best they serve to control the disease
process.

6.  Therefore a reasonable goal of drug therapy is resolution of disease symptoms such that
the patient can carry on normal daily functions.
References:-
 Xavier RJ, Podolsky DK (2007). "Unravelling the pathogenesis of inflammatory bowel
disease.".
 Bennike, Tue (2014). "Biomarkers in inflammatory bowel diseases: Current status and
proteomics identification strategies".
 "Crohn's & Colitis Foundation of America".
 Guindi M, Riddell RH. (2004). "Indeterminate colitis". Journal of Clinical Pathology.
 Hanauer SB, Sandborn W (2001-03-01). "Management of Crohn's disease in
adults" (PDF). American Journal of Gastroenterology.