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While immunosuppression facilitates infection, the contribution of soft tissues to infection beyond providing a portal for bacterial entry remains unclear. We showed previously that glutathione\n                    <jats:italic>S<\/jats:italic>\n                    \u2010transferase S1 (\n                    <jats:italic>gstS1<\/jats:italic>\n                    ), an enzyme with conjugating activity against the lipid peroxidation byproduct 4\u2010hydroxynonenal (4HNE), is important for resistance against wound infection in\n                    <jats:italic>Drosophila<\/jats:italic>\n                    muscle. The importance of the mammalian functional counterpart of\n                    <jats:italic>GstS1<\/jats:italic>\n                    in the context of wounds and infection has not been investigated. Here we demonstrate that the presence of a burn wound dramatically affects expression of both human\n                    <jats:italic>(hGSTA4)<\/jats:italic>\n                    and mouse\n                    <jats:italic>(mGsta4)<\/jats:italic>\n                    4HNE scavengers.\n                    <jats:italic>hGSTA4<\/jats:italic>\n                    is down\u2010regulated significantly within 1 wk of thermal burn injury in the muscle and fat tissues of patients from the large\u2010scale collaborative Inflammation and the Host Response to Injury multicentered study. Similarly,\n                    <jats:italic>mGsta4<\/jats:italic>\n                    , the murine GST with the highest catalytic efficiency for 4HNE, is down\u2010regulated to approximately half of normal levels in mouse muscle immediately postburn. Consequently, 4HNE protein adducts are increased 4\u2010 to 5\u2010fold in mouse muscle postburn. Using an open wound infection model, we show that deletion of\n                    <jats:italic>mGsta4<\/jats:italic>\n                    renders mice more susceptible to infection with the prevalent wound pathogen\n                    <jats:italic>Pseudomonas aeruginosa<\/jats:italic>\n                    , while muscle\n                    <jats:italic>hGSTA4<\/jats:italic>\n                    expression negatively correlates with burn wound infection episodes per patient. Our data suggest that\n                    <jats:italic>hGSTA4<\/jats:italic>\n                    down\u2010regulation and the concomitant increase in 4HNE adducts in human muscle are indicative of susceptibility to infection in individuals with severely thermal injuries.\u2014Apidianakis, Y., Que, Y.\u2010A., Xu, W., Tegos, G. P., Zimniak, P., Hamblin, M. R., Tompkins, R. G., Xiao, W., Rahme, L. G. Down\u2010regulation of\n                    <jats:italic>glutatione S\u2010transferase \u03b1 4 (hGSTA4)<\/jats:italic>\n                    in the muscle of thermally injured patients is indicative of susceptibility to bacterial infection.\n                    <jats:italic>FASEB J.<\/jats:italic>\n                    26, 730\u2013737 (2012). www.fasebj.org\n                  <\/jats:p>","DOI":"10.1096\/fj.11-192484","type":"journal-article","created":{"date-parts":[[2011,10,28]],"date-time":"2011-10-28T23:45:45Z","timestamp":1319845545000},"page":"730-737","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":20,"title":["Down\u2010regulation of\n                    <i>glutatione S\u2010transferase \u03b1 4 (hGSTA4)<\/i>\n                    in the muscle of thermally injured patients is indicative of susceptibility to bacterial infection"],"prefix":"10.1096","volume":"26","author":[{"given":"Yiorgos","family":"Apidianakis","sequence":"first","affiliation":[{"name":"Department of Surgery Harvard Medical School  Boston Massachusetts USA"},{"name":"Department of Surgery Massachusetts General Hospital  Boston Massachusetts USA"},{"name":"Shriners Burn Institute  Boston Massachusetts USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yok\u2010Ai","family":"Que","sequence":"additional","affiliation":[{"name":"Department of Surgery Harvard Medical School  Boston Massachusetts USA"},{"name":"Department of Surgery Massachusetts General Hospital  Boston Massachusetts USA"},{"name":"Shriners Burn Institute  Boston Massachusetts USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Weihong","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Biochemistry Stanford University School of Medicine  Stanford California USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"George P.","family":"Tegos","sequence":"additional","affiliation":[{"name":"Department of Dermatology Harvard Medical School  Boston Massachusetts USA"},{"name":"Wellman Center for Photomedicine Massachusetts General Hospital  Boston Massachusetts USA"},{"name":"Department of Pathology University of New Mexico  Albuquerque New Mexico USA"},{"name":"Center for Molecular Discovery University of New Mexico  Albuquerque New Mexico USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Piotr","family":"Zimniak","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology University of Arkansas for Medical Sciences  Little Rock Arkansas USA"},{"name":"Central Arkansas Veterans Healthcare System  Little Rock Arkansas USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael R.","family":"Hamblin","sequence":"additional","affiliation":[{"name":"Department of Dermatology Harvard Medical School  Boston Massachusetts USA"},{"name":"Wellman Center for Photomedicine Massachusetts General Hospital  Boston Massachusetts USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ronald G.","family":"Tompkins","sequence":"additional","affiliation":[{"name":"Department of Surgery Harvard Medical School  Boston Massachusetts USA"},{"name":"Department of Surgery Massachusetts General Hospital  Boston Massachusetts USA"},{"name":"Shriners Burn Institute  Boston Massachusetts USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wenzhong","family":"Xiao","sequence":"additional","affiliation":[{"name":"Department of Surgery Harvard Medical School  Boston Massachusetts USA"},{"name":"Department of Surgery Massachusetts General Hospital  Boston Massachusetts USA"},{"name":"Department of Biochemistry Stanford University School of Medicine  Stanford California USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Laurence G.","family":"Rahme","sequence":"additional","affiliation":[{"name":"Department of Surgery Harvard Medical School  Boston Massachusetts USA"},{"name":"Department of Microbiology and Molecular Genetics Harvard Medical School  Boston Massachusetts USA"},{"name":"Department of Surgery Massachusetts General Hospital  Boston Massachusetts USA"},{"name":"Shriners Burn Institute  Boston Massachusetts USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2011,10,28]]},"reference":[{"key":"e_1_2_19_2_1","doi-asserted-by":"publisher","DOI":"10.1128\/CMR.19.2.403-434.2006"},{"key":"e_1_2_19_3_1","doi-asserted-by":"publisher","DOI":"10.1097\/SCS.0b013e318175b4f0"},{"key":"e_1_2_19_4_1","first-page":"1142","article-title":"Successful treatment of invasive burn wound infection with sepsis in patients with major burns","volume":"113","author":"Chai J.","year":"2000","journal-title":"Chin. 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