AI Article Synopsis
- The study investigated how dexamethasone, a glucocorticoid, affects mucosal immunity, specifically looking at bacterial adherence and IgA levels in Fischer rats.
- Rats were divided into two groups; one received saline and the other received dexamethasone, resulting in a significant drop in IgA levels and increased bacterial adherence in the dexamethasone group.
- The findings suggest that the use of glucocorticoids may impair mucosal defenses, leading to higher rates of bacterial translocation to lymph nodes.
Article Abstract
Adherence of bacteria to intestinal epithelial cells may be the crucial initiating event for translocation and is normally prevented by both specific (secretory IgA) and nonspecific (mucus, bacterial antagonism, desquamation) mucosal defense mechanisms. The purpose of this study was to examine the effect of dexamethasone administration on mucosal immunity; specifically bacterial adherence and IgA. Twenty Fischer rats were randomly assigned to two groups of 10 animals each. Group I received 0.5 mL saline injection intraperitoneally (IP); and group II, 0.8 mg/150 g body weight dexamethasone IP per day for 2 consecutive days. The cecum mesenteric lymph nodes, and bile were aseptically collected, and bacterial adherence, bacterial translocation, and IgA concentration were determined. Results indicate that, compared with saline-treated animals, dexamethasone-treated animals had a fall in IgA (54 +/- 24 versus 232 +/- 41 micrograms/mg protein), an increase in bacterial adherence (8.2 +/- 0.5 versus 3.4 +/- 0.6 cfu (log10)/g cecum), and an increased incidence of bacterial translocation to the mesenteric lymph nodes (60% versus 0%). These data suggest that glucocorticoids may promote bacterial translocation by impairment of mucosal IgA synthesis.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1358497 | PMC |
| http://dx.doi.org/10.1097/00000658-199112000-00012 | DOI Listing |
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