Enterohepatic circulation of bacterial chemotactic peptide in rats with experimental colitis

C H Hobson ¹, T J Butt , D M Ferry

⁰Wellcome Medical Research Institute, Dunedin, New Zealand.

Gastroenterology +

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April 1, 1988

View abstract on PubMed

Summary

Colitis significantly increases the biliary excretion of proinflammatory bacterial peptides in rats. This suggests these peptides may contribute to colon inflammation and associated liver disorders.

Area Of Science

Gastroenterology
Hepatology
Microbiology

Background

Hepatobiliary disorders frequently accompany colonic inflammation.
The exact mechanisms linking these conditions remain unclear.
Increased gut permeability allowing bacterial products into circulation is a potential pathway.

Purpose Of The Study

To investigate the metabolic fate of a specific proinflammatory bacterial peptide in rats with and without experimental colitis.
To determine if colonic inflammation alters the peptide's excretion into bile.

Main Methods

Rats with induced experimental colitis and healthy controls were used.
A radiolabeled proinflammatory peptide (N-formyl L-methionine L-leucine 125I-L-tyrosine) was instilled into colonic loops.
Radioactivity in gut, liver, blood, and bile was measured; bile was analyzed using HPLC.

Main Results

Biliary excretion of the intact peptide was significantly higher (eightfold increase) in rats with colitis compared to healthy rats.
An enterohepatic circulation of the peptide was demonstrated in rats.

Conclusions

Experimental colitis markedly enhances the biliary excretion of proinflammatory bacterial peptides.
These bacterial peptides may play a role in the pathophysiology of colonic inflammation and related hepatobiliary complications.

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