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  • Title: The role of NO in macrophage dysfunction at early stage after burn injury.
    Author: Luo G, Peng D, Zheng J, Chen X, Wu J, Elster E, Tadaki D.
    Journal: Burns; 2005 Mar; 31(2):138-44. PubMed ID: 15683683.
    Abstract:
    AIM: To explore the role of nitric oxide (NO) in macrophage dysfunction at early stage after burn injury. METHOD: Peritoneal macrophages were isolated and cultured from early stage burnt mice. NO production and inducible NO synthase (iNOS) expression in the macrophages were checked by the Greiss method and real-time PCR (TaqMan), respectively. l-Arginine, the substrate of NO producing, or N-monomethyl-l-arginine (l-NMMA), a competing blocker of NOS was administered to the culture, the changes of NO, TNF-alpha and PGE2 productions were measured, additionally the changes of the iNOS, TNF-alpha and COX-2 expression were assayed by real-time PCR. After that, the effects of l-arginine and l-NMMA were determined on burnt macrophage influencing the proliferation of normal splenic lymphocytes. RESULT: A large amount of NO was produced by macrophages from post burn hour 6 (6PBH) with a high level of iNOS expression. l-Arginine could increase NO production in a dosage-dependent manner, while l-NMMA attenuated NO production, but neither could affect iNOS expression. Moreover, l-arginine enhanced productions of both the latter produced TNF-alpha and PGE2 from burnt macrophages, and the expressions of TNF-alpha and COX-2 were improved significantly, while l-NMMA did reverse ways. It was found that macrophages from post burn hour 24 mice could inhibit Con A-stimulated normal splenic lymphocytes dramatically, l-NMMA could decrease this function significantly, but l-arginine could not influence the suppression. CONCLUSION: Our experiment indicated NO derived from burnt macrophage played a vital role in macrophage producing excessive TNF-alpha and PGE2, and suppressing lymphocyte function at early stage after burn injury.
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