PMID- 8637894 OWN - NLM STAT- MEDLINE DCOM- 19960710 LR - 20220330 IS - 0027-8424 (Print) IS - 1091-6490 (Electronic) IS - 0027-8424 (Linking) VI - 93 IP - 6 DP - 1996 Mar 19 TI - Pathogenesis of influenza virus-induced pneumonia: involvement of both nitric oxide and oxygen radicals. PG - 2448-53 AB - The role of nitric oxide (NO) in the pathogenesis of influenza virus-induced pneumonia in mice was investigated. Experimental influenza virus pneumonia was produced with influenza virus A/Kumamoto/Y5/67(H2N2). Both the enzyme activity of NO synthase (NOS) and mRNA expression of the inducible NOS were greatly increased in the mouse lungs; increases were mediated by interferon gamma. Excessive production of NO in the virus-infected lung was studied further by using electron spin resonance (ESR) spectroscopy. In vivo spin trapping with dithiocarbamate-iron complexes indicated that a significant amount of NO was generated in the virus-infected lung. Furthermore, an NO-hemoglobin ESR signal appeared in the virus-infected lung, and formation of NO-hemoglobin was significantly increased by treatment with superoxide dismutase and was inhibited by N(omega)-monomethyl-L-arginine (L-NMMA) administration. Immunohistochemistry with a specific anti-nitrotyrosine antibody showed intense staining of alveolar phagocytic cells such as macrophages and neutrophils and of intraalveolar exudate in the virus-infected lung. These results strongly suggest formation of peroxynitrite in the lung through the reaction of NO with O2-, which is generated by alveolar phagocytic cells and xanthine oxidase. In addition, administration of L-NMMA resulted in significant improvement in the survival rate of virus-infected mice without appreciable suppression of their antiviral defenses. On the basis of these data, we conclude that NO together with O2- which forms more reactive peroxynitrite may be the most important pathogenic factors in influenza virus-induced pneumonia in mice. FAU - Akaike, T AU - Akaike T AD - Department of Microbiology, Kumamoto University School of Medicine, Japan. FAU - Noguchi, Y AU - Noguchi Y FAU - Ijiri, S AU - Ijiri S FAU - Setoguchi, K AU - Setoguchi K FAU - Suga, M AU - Suga M FAU - Zheng, Y M AU - Zheng YM FAU - Dietzschold, B AU - Dietzschold B FAU - Maeda, H AU - Maeda H LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - Proc Natl Acad Sci U S A JT - Proceedings of the National Academy of Sciences of the United States of America JID - 7505876 RN - 0 (Enzyme Inhibitors) RN - 0 (Free Radicals) RN - 0 (Reactive Oxygen Species) RN - 11062-77-4 (Superoxides) RN - 27JT06E6GR (omega-N-Methylarginine) RN - 31C4KY9ESH (Nitric Oxide) RN - 82115-62-6 (Interferon-gamma) RN - 94ZLA3W45F (Arginine) RN - EC 1.14.13.39 (Nitric Oxide Synthase) SB - IM MH - Animals MH - Arginine/analogs & derivatives/pharmacology MH - Electron Spin Resonance Spectroscopy MH - Enzyme Induction MH - Enzyme Inhibitors/pharmacology MH - Free Radicals MH - Influenza A virus/pathogenicity MH - Interferon-gamma/physiology MH - Lung/metabolism MH - Male MH - Mice MH - Nitric Oxide/*metabolism MH - Nitric Oxide Synthase/antagonists & inhibitors/biosynthesis MH - Pneumonia, Viral/*physiopathology MH - Reactive Oxygen Species/*metabolism MH - Superoxides/metabolism MH - omega-N-Methylarginine PMC - PMC39817 EDAT- 1996/03/19 00:00 MHDA- 1996/03/19 00:01 PMCR- 1996/09/19 CRDT- 1996/03/19 00:00 PHST- 1996/03/19 00:00 [pubmed] PHST- 1996/03/19 00:01 [medline] PHST- 1996/03/19 00:00 [entrez] PHST- 1996/09/19 00:00 [pmc-release] AID - 10.1073/pnas.93.6.2448 [doi] PST - ppublish SO - Proc Natl Acad Sci U S A. 1996 Mar 19;93(6):2448-53. doi: 10.1073/pnas.93.6.2448.