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[Therapeutic effect of anti-CXCL1 neutralizing antibody on acute ulcerative colitis in mice]
Linglong Luo1, Xuemei Zhang2, Jing Wang1
1Department of Gastroenterology, Third Xiangya Hospital, Central South University, Changsha 410013; Hunan Key Laboratory of Nonresolving Inflammation and Cancer, Third Xiangya Hospital, Central South University, Changsha 410013, China.
Objective:
To evaluate the therapeutic effect of CXCL1 monoclonal antibody on dextra sulfate sodium (DSS)-induced acute ulcerative colitis (UC) in mice, and to elucidate its effect on the expressions of TNF-α, IFN-γ, IL-17 and IL-10 as well as neutrophil infiltration. Methods: Female BALB/c mice were randomly divided into a normal group (DSS-), a disease group (DSS+saline), an anti-CXCL1 antibody group (DSS+anti-CXCL1 Ab) and a treatment control group (DSS+IgG Ab). The DSS+saline, DSS+anti-CXCL1 Ab and DSS+anti-CXCL1 Ab groups were given 3.5% DSS solution as drinking water to induce acute intestinal inflammation, while the normal control was given distilled water freely. The DSS+anti-CXCL1 Ab mice were intraperitoneal injected with anti-CXCL1 Ab (4 mg/kg) on the 3rd and 6th day. Same amount of rat IgG Ab was given in the DSS+IgG Ab group. The normal group and the disease group were injected with 0.9% sodium chloride solution. The value of disease activity index (DAI) and the injury of colorectal tissue were measured. The levels of TNF-α, IFN-γ, IL-10 and IL-17 in colonic tissues of mice were detected by RT-PCR. Myeloperoxidase (MPO), a specific marker of neutrophils was measured by immunohistochemistry. Results: Compared with the normal control group, DAI score and colorectal injury score in the disease group were significantly increased, but the DAI and colorectal in the mice with acute ulcerative colitis tissue damage score were significantly reduced after anti-CXCL1 Ab intervention. Compared with the normal control group, mRNA levels of TNF-α, IFN-γ and IL-17 in the colorectal tissues were significantly elevated (P<0.05) in the disease group while the IL-10 was decreased; these effects were attenuated by anti-CXCL1 Ab intervention (P<0.05). Immunohistochemistry showed that the infiltration of neutrophils (MPO+) in the colon tissue was significantly increased in the disease group, while the anti-CXCL1 Ab treatment could significantly reduce the neutrophil infiltration in colon tissue (P<0.05). Conclusion: Anti-CXCL1 Ab relieves the progression of DSS-induced acute ulcerative colitis by suppressing proinflammatory expression and neutrophil infiltration.
Insights
This study shows that anti-CXCL1 monoclonal antibody treatment effectively reduces inflammation and tissue damage in dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice. The antibody therapy suppressed pro-inflammatory cytokine expression and decreased neutrophil infiltration, offering a potential therapeutic strategy for UC.
Area of Science:
- Immunology
- Gastroenterology
- Inflammation Research
Background:
- Ulcerative colitis (UC) is a chronic inflammatory bowel disease with limited therapeutic options.
- Chemokine (C-X-C motif) ligand 1 (CXCL1) plays a role in neutrophil recruitment and inflammation.
- Targeting CXCL1 may offer a novel therapeutic approach for UC.
Purpose of the Study:
- To evaluate the therapeutic efficacy of a CXCL1 monoclonal antibody in a mouse model of acute ulcerative colitis.
- To investigate the antibody's impact on key inflammatory mediators and neutrophil infiltration.
Main Methods:
- Acute ulcerative colitis was induced in mice using dextran sulfate sodium (DSS).
- Mice were treated with anti-CXCL1 antibody, IgG antibody, or saline.
- Disease activity index, colorectal tissue injury, pro-inflammatory cytokine (TNF-α, IFN-γ, IL-17, IL-10) mRNA levels, and neutrophil infiltration (MPO) were assessed.
Main Results:
- Anti-CXCL1 antibody treatment significantly reduced disease activity index and colorectal tissue damage compared to controls.
- The treatment attenuated elevated mRNA levels of TNF-α, IFN-γ, and IL-17, while increasing IL-10 levels.
- Neutrophil infiltration into colon tissue was significantly decreased following anti-CXCL1 antibody administration.
Conclusions:
- Anti-CXCL1 monoclonal antibody demonstrates therapeutic potential for DSS-induced acute ulcerative colitis.
- The mechanism involves suppressing pro-inflammatory cytokine expression and reducing neutrophil infiltration.
- Targeting CXCL1 represents a promising strategy for managing ulcerative colitis.
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