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Defect of Interferon γ Leads to Impaired Wound Healing through Prolonged Neutrophilic Inflammatory Response and Enhanced MMP-2 Activation.

Abstract：

:Interferon (IFN)-γ is mainly secreted by CD4+ T helper 1 (Th1), natural killer (NK) and NKT cells after skin injury. Although IFN-γ 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-γ affects wound healing. Full-thickness wounds were created on the backs of wild type (WT) C57BL/6 and IFN-γ-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-γKO 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-γKO than in WT mice, whereas expression levels of MMP-2 (gelatinase) mRNA were significantly greater in IFN-γKO than in WT mice. Moreover, under neutropenic conditions created with anti-Gr-1 monoclonal antibodies, wound closure in IFN-γKO mice was recovered through low MMP-2 expression levels. These results suggest that IFN-γ may be involved in the proliferation and maturation stages of wound healing through the regulation of neutrophilic inflammatory responses.

journal_name

Int J Mol Sci

journal_title

International journal of molecular sciences

authors

Kanno E,Tanno H,Masaki A,Sasaki A,Sato N,Goto M,Shisai M,Yamaguchi K,Takagi N,Shoji M,Kitai Y,Sato K,Kasamatsu J,Ishii K,Miyasaka T,Kawakami K,Imai Y,Iwakura Y,Maruyama R,Tachi M,Kawakami K

doi

10.3390/ijms20225657

subject

Has Abstract

pub_date

2019-11-12 00:00:00

issue

22

issn

1422-0067

pii

ijms20225657

journal_volume

20

pub_type

杂志文章

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