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However, the mechanisms resulting in suppression are not known. Here, the hypothesis that Gram-negative bacteria bind and retain AGs, which are introduced into the lung and interact with host defenses to affect bacterial killing, was tested. Following in vitro exposure of one of several, pathogenic Gram-negative bacteria to the AG antibiotics kanamycin or gentamicin, AGs were detected in bacterial cell pellets (up to 208\u00a0\u03bcg\/mL). Using inhibitors of AG binding and internalization, the bacterial outer membrane was implicated as the predominant kanamycin and gentamicin reservoir. Following intranasal administration of gentamicin-bound bacteria or gentamicin solution at the time of infection with live, AG-na\u00efve bacteria, gentamicin was detected in the lungs of infected mice (up to 8\u00a0\u03bcg\/g). Co-inoculation with gentamicin-bound bacteria resulted in killing of AG-na\u00efve bacteria by up to 3-log10, mirroring the effects of intranasal gentamicin treatment. In vitro killing of AG-na\u00efve bacteria mediated by kanamycin-bound bacteria required the presence of detergents or pulmonary surfactant, suggesting that increased bacterial killing inside the murine lung is facilitated by the detergent component of pulmonary surfactant. These findings demonstrate that Gram-negative bacteria bind and retain AGs that can interact with host-derived pulmonary surfactant to enhance bacterial killing in the lung. This may help explain why AGs appear to have unique efficacy in the lung and might expand their clinical utility.<\/jats:p>","DOI":"10.1093\/femsmc\/xtac016","type":"journal-article","created":{"date-parts":[[2022,5,13]],"date-time":"2022-05-13T23:04:20Z","timestamp":1652483060000},"source":"Crossref","is-referenced-by-count":4,"title":["Gram-negative bacteria act as a reservoir for aminoglycoside antibiotics that interact with host factors to enhance bacterial killing in a mouse model of pneumonia"],"prefix":"10.1093","volume":"3","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0106-2962","authenticated-orcid":false,"given":"Christiaan D M","family":"Wijers","sequence":"first","affiliation":[{"name":"Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center , 1161 21st Avenue South, Nashville, TN 37232, United States"},{"name":"Vanderbilt Institute for Infection, Immunology, and Inflammation, Vanderbilt University Medical Center , 1161 21st Avenue 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States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eric P","family":"Skaar","sequence":"additional","affiliation":[{"name":"Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center , 1161 21st Avenue South, Nashville, TN 37232, United States"},{"name":"Vanderbilt Institute for Infection, Immunology, and Inflammation, Vanderbilt University Medical Center , 1161 21st Avenue South, Nashville, TN 37232, United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lauren D","family":"Palmer","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Illinois Chicago , 835 South Wolcott Avenue, Chicago, IL 60612, United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael J","family":"Noto","sequence":"additional","affiliation":[{"name":"Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center , 1161 21st Avenue 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