Journal of Gastrointestinal & Digestive System
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India, being a developing country, bears an enormous disease burden of tuberculosis (TB). Average prevalence of
all forms of tuberculosis in India is estimated to be 5.05 per 1000 and tuberculosis of GI tract remains the sixth most frequent
form of extra-pulmonary TB. Mycobacterium tuberculosis (TB) destroys normal Collagen in lung tissues causing cavitation
and this immunopathology is mediated in part by Matrix Metalloproteinase-1 (MMP-1). MMP-1 has also been implicated in
the pathogenesis of Inflammatory Bowel Disease, especially Crohn?s disease. There are no studies, however, regarding the role of
MMPs-1 in intestinal TB. A cross-sectional study was carried out in a tertiary care center to study the distribution of Collagen
type I & III and expression of MMP-1 in intestinal tuberculosis.
Materials & methods:
In 30 cases of intestinal TB, lesional area (ulcer/ stricture/ perforation with granulomas) and their
resected ends (relatively normal, controls), collagen distribution was studied using Picrosirius red staining. MMP-1 expression
was determined using Streptavidin biotin method of immunostaining.
Total percent collagen was increased in the submucosa (p=0.005) in lesional areas along with a disarray of collagen
fibrils. Collagen type I & III was observed at the periphery of granulomas, leading to encapsulation. Confluent granulomas,
however, showed reduced deposition of collagen. MMP-1 expression was increased in the cells of the granulomas (p<0.01), most
of them showing moderate to intense immunostaining. Fibroblasts, giant cells, epithelioid cells, macrophages and inflammatory
cells had an increased MMP-1 expression. Cases with perforation showed an inverse correlation between collagen distribution &
MMP-1 expression, suggesting the role of MMP-1 in degradation of collagen in these areas.
Intestinal TB shows an increased MMP-1 expression and distribution of Collagen type I & III I the submucosa.
Encapsulation of the granulomas occurs, possibly in an attempt to establish a latent infection and there is disarray in the collagen
fibrils deposition. A larger sample size could possibly establish an inverse correlation between the two.
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