{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,24]],"date-time":"2026-01-24T06:53:31Z","timestamp":1769237611430,"version":"3.49.0"},"reference-count":19,"publisher":"Microbiology Society","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2013,11,1]]},"abstract":"<jats:p>\n                  <jats:italic>Acinetobacter baumannii<\/jats:italic> is a Gram-negative bacterium that opportunistically infects critically ill hospitalized patients with breaches in skin integrity and airway protection, leading to significant morbidity and mortality. Considering the paucity of well-established animal models of immunosuppression to study <jats:italic>A. baumannii<\/jats:italic> pathogenesis, we set out to characterize a murine model of immunosuppression using the alkylating agent cyclophosphamide (CYP). We hypothesized that CYP-induced immunosuppression would increase the susceptibility of C57BL\/6 mice to developing <jats:italic>A. baumannii<\/jats:italic>-mediated pneumonia followed by systemic disease. We demonstrated that CYP intensified <jats:italic>A. baumannii<\/jats:italic>-mediated pulmonary disease, abrogated normal immune cell function and led to altered pro-inflammatory cytokine release. The development of an animal model that mimics <jats:italic>A. baumannii<\/jats:italic> infection onset in immunosuppressed individuals is crucial for generating novel approaches to patient care and improving public health strategies to decrease exposure to infection for individuals at risk.<\/jats:p>","DOI":"10.1099\/jmm.0.060004-0","type":"journal-article","created":{"date-parts":[[2013,9,3]],"date-time":"2013-09-03T04:10:50Z","timestamp":1378181450000},"page":"1747-1754","source":"Crossref","is-referenced-by-count":41,"title":["Characterization of a cyclophosphamide-induced murine model of immunosuppression to study Acinetobacter baumannii pathogenesis"],"prefix":"10.1099","volume":"62","author":[{"given":"Swetha","family":"Manepalli","sequence":"first","affiliation":[{"name":"Department of Biomedical Sciences, Long Island University-Post, Brookville, NY, USA"}]},{"given":"Jay A.","family":"Gandhi","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences, Long Island University-Post, Brookville, NY, USA"}]},{"given":"Vaibhav V.","family":"Ekhar","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences, Long Island University-Post, Brookville, NY, USA"}]},{"given":"Melissa B.","family":"Asplund","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences, Long Island University-Post, Brookville, NY, USA"}]},{"given":"Carolina","family":"Coelho","sequence":"additional","affiliation":[{"name":"PhD Program in Experimental Biology and Biomedicine, Centre for Neuroscience and Cell Biology of Coimbra and Institute of Microbiology, Faculty of Medicine, University of Coimbra, Coimbra, Portugal"},{"name":"Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY, USA"}]},{"given":"Luis R.","family":"Martinez","sequence":"additional","affiliation":[{"name":"Department of Medicine (Division of Infectious Diseases), Albert Einstein College of Medicine, Bronx, NY, USA"},{"name":"Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY, USA"},{"name":"Department of Biomedical Sciences, Long Island University-Post, Brookville, NY, USA"}]}],"member":"345","reference":[{"key":"r1","doi-asserted-by":"publisher","DOI":"10.1128\/JB.00834-08"},{"key":"r2","doi-asserted-by":"publisher","DOI":"10.1128\/JCM.40.2.685-686.2002"},{"key":"r3","doi-asserted-by":"publisher","DOI":"10.1099\/jmm.0.46747-0"},{"key":"r5","doi-asserted-by":"publisher","DOI":"10.1002\/eji.200324181"},{"key":"r6","doi-asserted-by":"publisher","DOI":"10.1021\/bi026110v"},{"key":"r7","first-page":"555","article-title":"Immunological reactivity of the lung. 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