Pro-inflammatory chemokine CCL2 (MCP-1) promotes healing in diabetic wounds by restoring the macrophage response.
Pro-inflammatory chemokine CCL2 (MCP-1) promotes healing in diabetic wounds by restoring the macrophage response.
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促炎趋化因子 CCL2 (MCP-1) 通过恢复巨噬细胞反应来促进糖尿病伤口的愈合。
DOI:
10.1371/journal.pone.0091574
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发表时间:
2014
期刊:
影响因子:
3.7
通讯作者:
Shafikhani SH
中科院分区:
文献类型:
--
作者:
Wood S;Jayaraman V;Huelsmann EJ;Bonish B;Burgad D;Sivaramakrishnan G;Qin S;DiPietro LA;Zloza A;Zhang C;Shafikhani SH
Prior studies suggest that the impaired healing seen in diabetic wounds derives from a state of persistent hyper-inflammation characterized by harmful increases in inflammatory leukocytes including macrophages. However, such studies have focused on wounds at later time points (day 10 or older), and very little attention has been given to the dynamics of macrophage responses in diabetic wounds early after injury. Given the importance of macrophages for the process of healing, we studied the dynamics of macrophage response during early and late phases of healing in diabetic wounds. Here, we report that early after injury, the diabetic wound exhibits a significant delay in macrophage infiltration. The delay in the macrophage response in diabetic wounds results from reduced Chemokine (C-C motif) ligand 2 (CCL2) expression. Importantly, one-time treatment with chemoattractant CCL2 significantly stimulated healing in diabetic wounds by restoring the macrophage response. Our data demonstrate that, rather than a hyper-inflammatory state; the early diabetic wound exhibits a paradoxical and damaging decrease in essential macrophage response. Our studies suggest that the restoration of the proper kinetics of macrophage response may be able to jumpstart subsequent healing stages. CCL2 chemokine-based therapy may be an attractive strategy to promote healing in diabetic wounds.
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影响因子:
2.9
作者:
DiPietro, LA;Reintjes, MG;Gamelli, RL
通讯作者:
Gamelli, RL
影响因子:
10.3
作者:
Fang, Y.;Shen, J.;Bao, S.
通讯作者:
Bao, S.
影响因子:
4.4
作者:
Ishida, Yuko;Gao, Ji-Liang;Murphy, Philip M.
通讯作者:
Murphy, Philip M.
影响因子:
4.4
作者:
Lucas, Tina;Waisman, Ari;Eming, Sabine A.
通讯作者:
Eming, Sabine A.
DOI:
10.4049/jimmunol.1101580
发表时间:
2012-04-15
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Kohlhapp FJ;Zloza A;O'Sullivan JA;Moore TV;Lacek AT;Jagoda MC;McCracken J;Cole DJ;Guevara-Patiño JA
通讯作者:
Guevara-Patiño JA