Jacoby D B, Choi A M
Division of Pulmonary and Critical Care Medicine, Johns Hopkins Asthma and Allergy Center, Baltimore, MD 21224.
Free Radic Biol Med. 1994 Jun;16(6):821-4. doi: 10.1016/0891-5849(94)90198-8.
Influenza infections cause airway epithelial inflammation and oxidant-mediated damage. In this setting, cellular antioxidant enzymes may protect airway epithelial cells against damage resulting from toxic oxygen radicals produced by activated leukocytes. Therefore, we tested the effect of influenza virus infection, as well as exposed to human recombinant interferon-gamma (IFN-gamma), on gene expression for the antioxidant enzymes manganese superoxide dismutase (MnSOD), copper/zinc superoxide dismutase (Cu/ZnSOD), indoleamine 2,3-dioxygenase (IDO), and catalase in primary cultures of human airway epithelial cells. In these cells, both viral infection and IFN-gamma increased MnSOD and IDO mRNAs. In contrast, neither viral infection nor IFN-gamma affected Cu/ZnSOD gene expression, and both viral infection and IFN-gamma decreased catalase gene expression. The differential effects of viral infection on antioxidant gene expression and their further amplification by IFN-gamma are likely to be important protective mechanisms in viral airway infections.
流感感染会引发气道上皮炎症和氧化应激介导的损伤。在这种情况下,细胞抗氧化酶可能保护气道上皮细胞免受活化白细胞产生的有毒氧自由基所导致的损伤。因此,我们测试了流感病毒感染以及暴露于重组人γ干扰素(IFN-γ)对人气道上皮细胞原代培养物中抗氧化酶锰超氧化物歧化酶(MnSOD)、铜/锌超氧化物歧化酶(Cu/ZnSOD)、吲哚胺2,3-双加氧酶(IDO)和过氧化氢酶基因表达的影响。在这些细胞中,病毒感染和IFN-γ均增加了MnSOD和IDO的mRNA水平。相反,病毒感染和IFN-γ均未影响Cu/ZnSOD基因表达,且病毒感染和IFN-γ均降低了过氧化氢酶基因表达。病毒感染对抗氧化基因表达的不同影响及其被IFN-γ的进一步放大,可能是病毒气道感染中的重要保护机制。