| First Author | Kanno E | Year | 2019 |
| Journal | Int J Mol Sci | Volume | 20 |
| Issue | 22 | PubMed ID | 31726690 |
| Mgi Jnum | J:290620 | Mgi Id | MGI:6435416 |
| Doi | 10.3390/ijms20225657 | Citation | Kanno E, et al. (2019) Defect of Interferon gamma Leads to Impaired Wound Healing through Prolonged Neutrophilic Inflammatory Response and Enhanced MMP-2 Activation. Int J Mol Sci 20(22):5657 |
| abstractText | Interferon (IFN)-gamma is mainly secreted by CD4+ T helper 1 (Th1), natural killer (NK) and NKT cells after skin injury. Although IFN-gamma is well known regarding its inhibitory effects on collagen synthesis by fibroblasts in vitro, information is limited regarding its role in wound healing in vivo. In the present study, we analyzed how the defect of IFN-gamma affects wound healing. Full-thickness wounds were created on the backs of wild type (WT) C57BL/6 and IFN-gamma-deficient (KO) mice. We analyzed the percent wound closure, wound breaking strength, accumulation of leukocytes, and expression levels of COL1A1, COL3A1, and matrix metalloproteinases (MMPs). IFN-gammaKO mice exhibited significant attenuation in wound closure on Day 10 and wound breaking strength on Day 14 after wound creation, characteristics that are associated with prolonged neutrophil accumulation. Expression levels of COL1A1 and COL3A1 mRNA were lower in IFN-gammaKO than in WT mice, whereas expression levels of MMP-2 (gelatinase) mRNA were significantly greater in IFN-gammaKO than in WT mice. Moreover, under neutropenic conditions created with anti-Gr-1 monoclonal antibodies, wound closure in IFN-gammaKO mice was recovered through low MMP-2 expression levels. These results suggest that IFN-gamma may be involved in the proliferation and maturation stages of wound healing through the regulation of neutrophilic inflammatory responses. |
