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CXCR2 may be critical in recruiting neutrophils (PMN) into the inflamed colon in DSS‐induced colitis
Author(s) -
Shukkur Farooq Muhammed,
Stillie RoseMarie,
Rostom Reem,
Svensson Majlis,
Svanborg Catharina,
Streiter Robert M.,
Stadnyk Andrew W.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1120.7
Subject(s) - colitis , submucosa , medicine , infiltration (hvac) , inflammatory bowel disease , crypt , edema , gastroenterology , immunology , pathology , disease , physics , thermodynamics
Dextran sodium sulphate (DSS)‐induced colitis in mice is characterized by PMN infiltration into the colonic mucosa and lumen. The mechanism by which this occurs is unclear. To address this, we determined the role of CXCR2 in DSS‐induced colitis by neutralizing CXCR2 or using CXCR2 KO (knockout) mice. DSS (5% w/v) was administered through drinking water to CXCR2 KO and Balb/c mice (WT) for 5 days followed by tap water for 1 day. In the neutralization study, DSS‐treated or control WT mice were injected i.p with goat serum or goat anti‐CXCR2 serum and disease severity was assessed. DSS‐treated CXCR2 KO mice failed to recruit PMN into the mucosa and had less severe crypt damage with no ulceration compared with WT mice. In the neutralization experiments, goat serum‐injected mice receiving DSS lost weight and showed severe clinical illness. Histological observation revealed edema, PMN infiltration into the submucosa and mucosa, extensive crypt damage with abscesses, and ulceration. In contrast, the anti‐CXCR2 serum‐treated mice showed less clinical illness with no weight loss. This was associated with less histological damage and a lack of PMN infiltration. Our experiments suggest a role for CXCR2 in DSS‐induced colitis and that it may be critical in recruiting PMN into the inflamed mucosa. Funded by the CCFC and the Swedish Medical Research Council, and an IWK Health Centre Fellowship to SMF.