Pleural Fluid Regulates Metabolism and Cytotoxicity in Acinetobacter baumannii to Augment Host Immune Responses

RODMAN, NYAH; JUN NAKANOUCHI; EMILY DANG; ANTHONY M. MENDOZA; CATHERINE A. BRENNAN; MARIA SOLEDAD RAMIREZ; MARTINEZ, JASMINE; AMBER L. MYERS; FERNANDEZ, JENNIFER S.; VERONICA JIMENEZ; BONOMO, ROBERT A.; SAMMIE FUNG; CAITLIN M. HARRIS; CHRISTINE LIU; NIKOLAS NIKOLAIDIS; RODRIGO SIEIRA

Congreso; ASM Microbe 2019; 2019

Acinetobacter baumannii is a notorious nosocomial pathogen with mortality rates among patients in intensive care units reported between 21.6-67%. A. baumannii is responsible for a high number of health-care associated cases of pneumonia, bacteremia, and urinary, skin, or surgical-derived infections. This bacterium has also garnered considerable clinical significance as a result of its intrinsic antibiotic resistance mechanisms, innate ability to persist for long periods upon desiccation and starvation, and capability to acquire foreign resistance determinants from the surrounding environment. Apart from its dynamic antibiotic resistance, A. baumannii has also been shown to be extremely persistent under many conditions. Modifications in metabolism and nutritional needs have been linked to the ability of A. baumannii to persist and adapt to a hostile host environment. Human serum albumin (HSA), the main blood protein component and an important marker of host nutritional and inflammatory status, triggers the differential expression of a number of key genes involved in the survival and persistence of A. baumannii. Pleural fluid (PF), an HSA-containing medium which primarily functions to lubricate pleurae during respiratory movements, is continuously produced by intercostal arteries and removed by the lymphatic system. Disruption of this flow can result in an abnormal amount of fluid in the chest cavity known as a pleural effusion, a frequent sign of underlying disease to which bacterial pneumonia constitutes the second leading cause in the United States with an annual incidence of 300,000. Accordingly, PF constitutes a host component that this nosocomial pathogen is in many instances obliged to cope with. We hypothesize that PF provides a diverse set of environmental cues for bacterial adaptation to harsh conditions within the host.