Intestinal mucus protects the underlying epithelium against adhesion and invasion by microbial pathogens and their products. In inflamed colonic mucosa there are both histochemical and biochemical changes in the major organic constituent of mucus, goblet cell-derived
mucin. To determine if these changes result in differences in functional properties of
mucin, inhibition of adherence of piliated Escherichia coli, strain RDEC-1 (serotype O15:H-), by
mucin purified from distal colons of normal rabbits was compared with inhibition by
mucin from colons of rabbits with
dinitrochlorobenzene-induced
colitis. Histology from inflamed colons revealed evidence of chronicity with a chronic inflammatory cell infiltrate, depletion of mucous glands, and branching of crypts.
Mucin was purified from crude mucus of distal colonic mucosa by sequential ultracentrifugation and characterized by gel electrophoresis and
amino acid analysis. The rabbit enteropathogen RDEC-1 was grown to promote expression of adherence pili. A nonpiliated mutant, strain M34, was used as a negative control. A concentration-dependent inhibition of piliated RDEC-1 binding was shown using
mucins derived from both inflamed and noninflamed colons. However, equivalent dry weights of
mucin purified from inflamed colons showed less inhibition of bacterial binding (10.3% inhibition +/- 5.2%; mean +/- SD) compared with
mucin from normal colons (47.6% +/- 10.8%; P less than 0.05).
Mucin purified from additional animals with
hapten-induced
colitis but treated with the oral
leukotriene B4-receptor antagonist
SC-41930 showed intermediate inhibition of RDEC-1 binding (35.6% +/- 14.3%). It is concluded that
mucin derived from inflamed distal colon of rabbits failed to inhibit in vitro binding of piliated RDEC-1, and by decreasing mucosal
inflammation, this functional alteration of
mucin was partially reversed.