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  Indian J Med Microbiol
 

Figure 1: Schematic representation of molecular and cellular mechanism in the development of IBD. (1) Factors including environmental factors, genetic factors, lifestyle etc. affect the intestinal microbiota, which further activate the immune cells and create the inflammatory machinery. (2) The inflammatory molecules cross the epithelial barrier and form crypt abscesses, (3) which facilitate the invasion of microbes that stimulate the inflammatory cytokines. (4) The fluctuations in the expression of pro-inflammatory and anti-inflammatory cytokines that leads to failure of epithelial barrier function. (5) Reduction of anti-inflammatory cytokines, which results in loss of tolerance to antigens of naïve microbiota, and facilitates the continuation of the inflammatory process. *In CD, T- helper 1 cells are involved and increase in IFN- γ , TNF- α , and IL-2 can be observed. Whereas, ××in UC, increased production of IL-4, IL-5, IL- 13 and IL-1 β was observed with the action of T- helper 2 cells.

Figure 1: Schematic representation of molecular and cellular mechanism in the development of IBD.
(1) Factors including environmental factors, genetic factors, lifestyle <i>etc</i>. affect the intestinal microbiota, which further activate the immune cells and create the inflammatory machinery. (2) The inflammatory molecules cross the epithelial barrier and form crypt abscesses, (3) which facilitate the invasion of microbes that stimulate the inflammatory cytokines. (4) The fluctuations in the expression of pro-inflammatory and anti-inflammatory cytokines that leads to failure of epithelial barrier function. (5) Reduction of anti-inflammatory cytokines, which results in loss of tolerance to antigens of naïve microbiota, and facilitates the continuation of the inflammatory process. <sup>*</sup>In CD, T- helper 1 cells are involved and increase in IFN- γ , TNF- α , and IL-2 can be observed. Whereas, <sup>××</sup>in UC, increased production of IL-4, IL-5, IL- 13 and IL-1 β was observed with the action of T- helper 2 cells.