Disruption of intestinal barrier function associated with experimental colitis: possible role of mast cells

Abstract

The objective was to characterize changes in barrier and transport function in an experimental model of colitis, and to determine whether mast cells contribute to these changes. Colitis was induced in rats with intracolonic 2,4,6-trinitrobenzenesulfonic acid (TNBS, 30 mg) in 50% ethanol. Controls received 0.9% saline or the ethanol vehicle alone. In vivo loop perfusion was used to assess colonic water flux (in μl ⋅ cm−1 ⋅ h−1) and lumen-to-blood 51Cr-labeled EDTA clearance (% administered dose) after TNBS. Myeloperoxidase (MPO) was used as an index of granulocyte influx. TNBS or its vehicle caused a marked decrease in water absorption and an increase in permeability at 4 h after administration compared with saline. Neither dexamethasone (anti-inflammatory control) nor doxantrazole (mast cell stabilizer) was able to attenuate these early changes likely caused by the vehicle. In contrast, at later times, TNBS (but not its vehicle) also increased51Cr-EDTA permeability and decreased water absorption; both effects were significantly attenuated by dexamethasone or doxantrazole. These drugs also significantly reduced TNBS-induced MPO accumulation and release of rat mast cell protease II. We conclude that experimental colitis is associated with severe defects in intestinal transport and barrier functions and that mast cells may contribute to the pathogenesis of these changes.

The anti-translocation and anti-inflammatory effect of cinnamon oil in mice with TNBS induced colitis

“…In our preliminary experiments, we found negative cytotoxic effects of higher concentration of cinnamon essential oil on intestinal cells (Fabián et al 2006). TNBS administration causes extensive colonic damage associated with marked defects in epithelial barrier and changes of intestinal permeability (Stein et al 1998). Huang et al 1993 reported that mucosal permeability increases because of mucosal atrophy in burns and this causes bacterial translocation.…”

Lack of flagella disadvantages Salmonella enterica serovar Enteritidis during the early stages of infection in the rat

“…MPO levels in the rat small intestine were unchanged 24 h after infection with S. Enteritidis S1400 but were significantly elevated at 72 h. Intestine tissue water content and faecal elastase was also increased at 72 h. This suggests that active recruitment of neutrophils to the intestine (Darwin & Miller, 1999;Stein et al, 1998;Faro et al, 2000;Zimmerman & Granger, 1990;McCormick et al, 1995;Naughton et al, 1996a) may have occurred between 24 and 72 h p.i. These changes would be consistent with the infiltration of polymorphonuclear leukocytes and other inflammatory cells into gut tissue and the release of inflammatory cells into the lumen, previously observed in vivo (Naughton et al, 1995(Naughton et al, , 1996a.…”

“…Freeze-dried intestine samples were homogenized (1 : 20, w/v) in ice-cold 0·5 M potassium phosphate (pH 6·0) containing hexadecyltrimethylammonium bromide (HETAB, 5 g l À1 ) and EDTA (3·72 g l À1 ) (Stein et al, 1998;Faro et al, 2000). They were left on ice for 60 min and then centrifuged (3000 g, 30 min, 4 8C).…”

Balsalazine decreases intestinal mucosal permeability of dextran sulfate sodium-induced colitis in mice

“…However, whether balsalazine improves intestinal mucosal permeability is still unknown [15,16] . [17,18] . Therefore, dextran sulfate sodium (DSS)-induced colitis is considered an appropriate model of the injured mucosal barrier [19] .…”