Journal of Clinical Pathology and Laboratory Medicine

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Opinion Article - Journal of Clinical Pathology and Laboratory Medicine (2023) Volume 5, Issue 2

Inflammation of the bowels: immunopathology

Michael Panwar*

Department of Biological Sciences,University of Amsterdam, Netherlands.

*Corresponding Author:
Michael Panwar
Department of Biological Sciences
University of Amsterdam

Received:27-Feb-2023, Manuscript No. AACPLM-23-90183; Editor assigned:01-Mar-2023, PreQC No. AACPLM-23-90183(PQ); Reviewed:15-Mar-2023, QC No. AACPLM-23-90183; Revised:21-Mar-2023, Manuscript No. AACPLM-23-90183(R); Published:28-Mar-2023, DOI:10.35841/aacplm-5.2.138

Citation: Panwar M. Inflammation of the bowels: Immunopathology. J Clin Path Lab Med. 2023;5(2):138


The immune system, the environment, and susceptibility genes interact in a complicated series of ways that lead to Inflammatory Bowel Disease (IBD). Viernes, fungus, and the host microbiome all contribute significantly to the onset of IBD, either directly by inducing inflammation or indirectly through changes in the immune system. Researchers can now quantify the diverse microbiome components, which will enable further advancements in the understanding of the genesis of IBD. IBD's pathogenesis has been linked to a number of mucosal immune system elements, including intestinal epithelial cells, innate lymphoid cells, cells of the innate and adaptive immune systems, and their secreted mediators. A mucosal vulnerability or a flaw in the sampling of gut luminal antigen results in the activation of the innate immune system, which may be mediated by increased toll-like receptor activity. Naive T-cells are subsequently mediated by the antigen-presenting cells to differentiate into effector T helper (Th) cells, such as Th1, Th2, and Th17, which disrupt gut homeostasis and cause IBD.


Inflammatory bowel disease, Crohn’s disease, Ulcerative colitis, Innate lymphoid cells, Adaptive immune system.


The chronic inflammatory disorder known as Inflammatory Bowel Disease (IBD), which includes Ulcerative Colitis (UC) and Crohn's Disease (CD), is characterized by alternating episodes of clinical remission and relapse. In addition to exhaustion, chronic diarrhea with or without extensive bleeding, abdominal pain, weight loss, and fever, CD can affect any region of the gastrointestinal tract. UC typically affects the colon and manifests as lower abdominal pain, tenesmus, rectal bleeding, frequent faeces, and mucus discharge from the rectum. In the context of a genetically vulnerable person, a dysregulated immune system is assumed to be the cause of IBD. 1.4 million Americans currently suffer from IBD, which has a prevalence rate of 396 per 100,000 people worldwide[1].

Combination of a patient's genetic makeup, microbiome, immune system, and environmental factors that cause genetically vulnerable people to have an overactive and aberrant immune reaction against commensal bacteria. Epidemiological evidence points to a connection between IBD and several environmental factors, including the use of antibiotics, microbial exposure both early and late in life, and probably diet. IBD is assumed to have a complex and polygenic genetic makeup. IBD may arise as a result of dysregulation in innate and adaptive immunity, according to genome-wide association studies. Genes linked to autophagy (ATG16L1), the interleukin (IL)-23/Th17 pathway, the TGF-beta pathway, and T-cell activation, among other immune system genes, have been shown to harbour susceptibility variations[2].

Researchers have been able to ascertain the microbiome's composition using metagenomics sequencing and the 16S ribosomal RNA (rRNA) gene. Several studies have recently characterized the "normal" human gut microbiome. Briefly, it is estimated that Bacteroidetes and Firmicutes together account for more than 90% of all phenotypes. Additional divisions, including as Proteobacteria, Actinobacteria, Fusobacteria, and Verrucomicrobia, have routinely been found in "normal" people. According to theory, the resilience of the faecal microbiota, which is thought to be generally consistent throughout time, changes only briefly in response to exposure to food, medication, and the external environment[3].

The process of "self-eating," also known as autophagy, causes organelles, unfolded proteins, or foreign extracellular material to be degraded by lysosomes. It is an essential procedure needed to keep cells in a state of homeostasis following an infection, mitochondrial damage, or ER stress. Pathological inflammation has been linked to deficiencies in autophagy, and GWAS has connected two important autophagy genes, ATG16L1 and IRGM, to CD. It has been demonstrated that Paneth cell granule anomalies in an ATG16L1 hypomorphic mouse strain, which expresses about 1% of the normal level of ATG16L1, are comparable to those seen in ideal resections in CD patients who also possess the ATG16L1 gene variation. Although these hypomorphic ATG16L1 mice do not experience spontaneous colitis, it was discovered that they are more vulnerable to DSS colitis[4].

As a defense against a variety of infectious pathogens, the immune system has developed. The innate and adaptive immune responses make up the two main effector types of the immune system in vertebrates. The innate immune system serves as the body's initial line of defense against infections and offers a quick protective reaction. It also aids in the start of the adaptive immune response. Innate immunity is non-specific and does not provide long-lasting protection. The epithelial barrier, macrophages, monocytes, neutrophils, DCs, natural killer cells, eosinophils, and basophils make up the innate immune system. By secreting cytokines, chemokines, and antimicrobial substances, these cells work in concert to start an inflammatory response. As a result, infected cells and bacteria are phagocytosed, antigens are presented, and the adaptive immune system is activated[5].


The pathophysiology of IBD is now being linked to new Th cell subsets, including follicular helper T-cells, IL-22-producing Th22 cells, IL-9-producing Th9 cells, and emerging forms of Treg cells. Also, it was often believed that terminally differentiated T cells seldom underwent re-differentiation into other T cell subsets; nevertheless, the plasticity of T cells is currently the subject of substantial research. The importance of the adaptive immune system in the initiation and maintenance of the inflammatory cascade in Inflammatory Bowel Disease (IBD) has been well established. T-cells in particular have been found to play a significant role in promoting intestinal inflammation. The significance of the innate immune system in the pathobiology of IBD has been made clear by recent developments. Beside anti-TNF medications, compounds that target certain T-cell generated molecules have mainly failed. This demonstrates how unique each person's immune system is in the setting of their own genetics and is probably owing to the complexity and redundancy of cytokine networks. Studies of the relationships between the various innate and adaptive immune system components, as well as the relationships with the intestinal microbiota, and how these relationships relate in the dominant context of an individual's genetics, will open new vistas in our understanding of the mechanisms underlying gut inflammation.


  1. Lakatos PL. Recent trends in the epidemiology of inflammatory bowel diseases: up or down?.World J Gastroenterol. 2006;12:6102-8.
  2. Indexed at, Google Scholar, Cross Ref

  3. Lichtenstein GR, Hanauer SB, Sandborn WJ. Management of Crohn’s disease in adults.Am J Gastroenterol. 2009;104:465-83.
  4. Indexed at, Google Scholar,

  5. Satsangi J, Silverberg MS, Vermeire S, et al. The Montreal classification of inflammatory bowel disease: controversies, consensus, and implications.Gut. 2006; 55:749-753.
  6. Indexed at, Google Scholar, Cross Ref

  7. Kornbluth A, Sachar DB. Ulcerative colitis practice guidelines in adults . Am J Gastroenterol. 1997; 92:204-211.
  8. Indexed at, Google Scholar, Cross Ref

  9. Bernstein CN, Wajda A, Blanchard JF. The clustering of other chronic inflammatory diseases in inflammatory bowel disease: A population-based study.Gastroenterology. 2005;129:827-836.
  10. Indexed at, Google Scholar, Cross Ref

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