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We provide evidence of a mechanism in human primary macrophages whereby the oxidative stress sensor Kelch-like ECH-associated protein 1 (Keap1) negatively regulates inflammatory responses and thus facilitates intracellular growth of\n                    <jats:italic>M. avium<\/jats:italic>\n                    . Our findings are of high biological and clinical significance, as opportunistic infections with nontuberculous mycobacteria are receiving renewed attention because of increased incidence and difficulties in treatment. Altered Keap1 gene expression may also have vital clinical implications for other inflammation-associated conditions, opening novel research venues for translational research, for instance in the expanding field of host-targeted therapy for infectious diseases.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1423449112","type":"journal-article","created":{"date-parts":[[2015,7,20]],"date-time":"2015-07-20T20:23:40Z","timestamp":1437423820000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":48,"title":["Keap1 regulates inflammatory signaling in\n                    <i>Mycobacterium avium<\/i>\n                    -infected human macrophages"],"prefix":"10.1073","volume":"112","author":[{"given":"Jane Atesoh","family":"Awuh","sequence":"first","affiliation":[{"name":"Centre of Molecular Inflammation Research, Norwegian University of Science and Technology, 7491 Trondheim, Norway;"},{"name":"Department of Cancer Research and 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