Wound healing in Mac‐1 deficient mice

Abstract

Mac-1 (CD11b/CD18) is a macrophage receptor that plays several critical roles in macrophage recruitment and activation. Because macrophages are essential for proper wound healing, the impact of Mac-1 deficiency on wound healing is of significant interest. Prior studies have shown that Mac-1−/− mice exhibit deficits in healing, including delayed wound closure in scalp and ear wounds. The current study examined whether Mac-1 deficiency influences wound healing in small excisional and incisional skin wounds. Three millimeter diameter full thickness excisional wounds and incisional wounds were prepared on the dorsal skin of Mac-1 deficient (Mac-1 −/−) and wild type (WT) mice, and wound healing outcomes were examined. Mac-1 deficient mice exhibited a normal rate of wound closure, generally normal levels of total collagen, and nearly normal synthesis and distribution of collagens I and III. In incisional wounds, wound breaking strength was similar for Mac-1 −/− and WT mice. Wounds of Mac-1 deficient mice displayed normal total macrophage content, although macrophage phenotype markers were skewed as compared to WT. Interestingly, amounts of TGF-β1 and its downstream signaling molecules, SMAD2 and SMAD3, were significantly decreased in the wounds of Mac-1 deficient mice compared to WT. The results suggest that Mac-1 deficiency has little impact on the healing of small excisional and incisional wounds. Moreover, the findings demonstrate that the effect of single genetic deficiencies on wound healing may markedly differ among wound models. These conclusions have implications for the interpretation of the many prior studies that utilize a single model system to examine wound healing outcomes in genetically deficient mice.

Comparing the influence of two immunosuppressants (fingolimod, azathioprine) on wound healing in a rat model of primary and secondary intention wound closure

“…Their increase in the azathioprine group indicates that the healing tissue of these animals was still in the stage of proliferation and not in the tissue remodeling stage, again suggesting that healing would be delayed in the azathioprine group. It has been described that macrophage‐deficient wounds show reduced angiogenesis, altered epithelization and failure in repair which corresponds to our findings in the azathioprine group. In the excisional model, there were no differences in the M2 macrophage count among the three groups because the healing process was more complex and reepithelialization had not yet been completed in any of the three groups, with the proliferation phase still being maintained.…”

Exploring the mechanism of Huanglian ointment in alleviating wound healing after anal fistula surgery through metabolomics and proteomics

“…Itgam and Itgb2 encode integrin αM and β2 chains, respectively, which together form the leukocyte-specific integrin called Mac-1 [ 63 ]. Mac-1 deficiency leads to recurrent severe infections, impaired pus formation, and wound healing defects [ 64 ]. Cttn, which encodes cortactin, a microfilament actin-binding protein, is involved in regulating the reshaping of the cytoskeleton.…”