Anti-Neutrophil Serum Attenuates Dextran Sulfate Sodium-Induced Colonic Damage in the Rat

Abstract

The data showing that anti-neutrophil serum attenuates distal colonic mucosal injury induced by dextran sulfate sodium support the hypothesis that neutrophils play a pathogenic role in this model of colonic mucosal damage.

Regulation of dextran sodium sulfate induced colitis by leukocyte beta 2 integrins

“…Second, due to a global gene targeted mutation, the genetic loss of CD11b may have more far reaching 47 Nonetheless, our data reveal a dichotomous role for different members of Previous studies have shown that DSS mediated colitis is largely due to increased neutrophil and monocyte recruitment, such that anti-neutrophil serum or blockade of monocyte infiltration significantly attenuates disease. 25,27 Our data also demonstrate that neutrophil recruitment is important for DSS colitis and that CD18 and CD11a play key roles in facilitating this process. This observation is surprising since many studies have reported that CD11b/CD18 (Mac-1) serves as the primary mediator of neutrophil-endothelial cell interactions and subsequent recruitment.…”

“…24,25 Immunopathogenesis of the DSS model involves multiple immune cell types implicated in human IBD including neutrophils and monocytes, with lymphocytes serving a regulatory role. 22,[25][26][27][28] Therefore, we used the DSS colitis model to determine the pathological role of leukocyte b 2 integrins during experimental colitis. Here, we report that gene targeted null deficiency of CD18 b 2 integrin and CD11a (a L integrin) significantly attenuates the development of DSS-induced colitis, and that loss of CD11b (a M chain) actually enhanced DSS-induced colitis.…”

The Role of Dendritic Cells in the Development of Acute Dextran Sulfate Sodium Colitis

“…Increased MIP-2 secretion has been associated with exacerbated DSS colitis both in an adiponectin KO model (41), and when epithelial cells were engineered to secrete MIP-2 (27). Our data indicate that in response to DSS, DCs directly contribute to the distinctive neutrophil involvement of this model of colitis (25). Moreover, DSS-activated DCs also produced Th1 cytokines and other attractants that may further exacerbate gut inflammation.…”

Human [Gly2]GLP-2 reduces the severity of colonic injury in a murine model of experimental colitis

“…Infusion of rat anti-neutrophil serum lowered the circulating neutrophil count, reduced mucosal damage, and stabilized, but did not prevent weight loss (17) and topical application of lidocaine, prednisolone, or sucralfate reduced mucosal permeability, in rats with DS-induced colitis (3). Neutralization of TNF by infusion of anti-TNF monoclonal or polyclonal antibodies either had no effect (41) or exacerbated the development of acute DS-induced colitis in mice (32), whereas infusion of homologous IgG or a 5-lipoxygenase activating protein inhibitor improved DS-induced colitis in rats and mice, respectively (38,45).…”