The tripeptide feG reduces endotoxin-provoked perturbation of intestinal motility and inflammation

Area of Science:

• Gastroenterology
• Immunology
• Pharmacology

Background:

• Lipopolysaccharide (LPS) induces intestinal endotoxaemia, disrupting gut motility and causing inflammatory cell influx.
• Rat submandibular gland peptide T (SGP-T) and its fragments (FEG, feG) are known to modulate intestinal anaphylactic reactions.

Purpose of the Study:

• To investigate the potential of SGP-T, FEG, and feG in modulating LPS-induced intestinal endotoxaemia in conscious rats.
• To assess the effects of these peptides on intestinal motility and inflammatory responses.

Main Methods:

• Rats were administered intravenous LPS to induce endotoxaemia.
• The effects of SGP-T, FEG, and feG on the disruption of migrating motor complexes (MMCs) were evaluated.
• Leukocyte extravasation and CD18 expression in mesenteric tissue were measured after LPS challenge.
• Oral administration of feG was used to assess its impact on late-phase inflammatory markers.

Main Results:

• All three peptides (SGP-T, FEG, feG) prevented the disruption of intestinal MMCs caused by LPS.
• Orally administered feG significantly reduced leukocyte extravasation into the peritoneal cavity.
• feG decreased the expression of the activation marker CD18 on mesenteric tissue leukocytes and intestinal tissue leukocytes.

Conclusions:

• The peptide feG effectively attenuates both immediate (intestinal motility) and late-phase (inflammatory cell influx and activation) reactions associated with LPS-induced endotoxaemia.
• feG demonstrates therapeutic potential for managing endotoxaemia-related gastrointestinal inflammation.