The role of MIP-1α in the development of systemic inflammatory response and organ injury following trauma hemorrhage

Chi Hsun Hsieh, Michael Frink, Ya Ching Hsieh, Wen Hong Kan, Jun Te Hsu, Martin G. Schwacha, Mashkoor A. Choudhry, Irshad H. Chaudry

Resultado de la investigación: Articlerevisión exhaustiva

61 Citas (Scopus)


Although MIP-1α is an important chemokine in the recruitment of inflammatory cells, it remains unknown whether MIP-1α plays any role in the development of systemic inflammatory response following trauma-hemorrhage (T-H). C57BL/6J wild type (WT) and MIP-1α-deficient (KO) mice were used either as control, subjected to sham operation (cannulation or laparotomy only or cannulation plus laparotomy) or T-H (midline laparotomy, mean blood pressure 35 ± 5 mmHg for 90 min, followed by resuscitation) and sacrificed 2 h thereafter. A marked increase in serum α-glutathione transferase, TNF-α, IL-6, IL-10, MCP-1, and MIP-1α and Kupffer cell cytokine production was observed in WT T-H mice compared with shams or control. In addition lung and liver tissue edema and neutrophil infiltration (myeloperoxidase (MPO) content) was also increased following T-H in WT animals. These inflammatory markers were markedly attenuated in the MIP-1α KO mice following T-H. Furthermore, compared with 2 h, MPO activities at 24 and 48 h after T-H declined steadily in both WT and KO mice. However, normalization of MPO activities to sham levels within 24 h was seen in KO mice but not in WT mice. Thus, MIP-1α plays an important role in mediating the acute inflammatory response following T-H. In the absence of MIP-1α, acute inflammatory responses were attenuated; rapidly recovered and less remote organ injury was noted following T-H. Thus, interventions that reduce MIP-1α levels following T-H should be useful in decreasing the deleterious inflammatory consequence of trauma.

Idioma originalEnglish (US)
Páginas (desde-hasta)2806-2812
Número de páginas7
PublicaciónJournal of Immunology
EstadoPublished - ago 15 2008

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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