Depletion of Alveolar Macrophages Increases Pulmonary Neutrophil Infiltration, Tissue Damage, and Sepsis in a Murine Model of Acinetobacter baumannii Pneumonia
Hiu Ham Lee, Lilit Aslanyan, Arjun Vidyasagar, Melissa B. Brennan, Maxine S. Tauber, Maria Alícia Carrillo-Sepúlveda, Michael R. Dores, Nathan W. Rigel, Luis R. Martinez
Abstract
Acinetobacter baumannii has emerged as an important etiological agent of hospital-related infections, especially nosocomial pneumonia. The virulence factors of this bacterium and their interactions with the cells and molecules of the immune system just recently began to be extensively studied. Here, we investigated the impact of alveolar macrophages on A. baumannii pneumonia using a mouse model of infection and a flexible tissue culture system. We hypothesized that depletion of macrophages would enhance sepsis and severity of A. baumannii disease.
Topics & Concepts
Acinetobacter baumanniiPneumoniaSepsisMicrobiologyBiologyVirulenceImmune systemImmunologyInfiltration (HVAC)BacteriaMedicinePseudomonas aeruginosaInternal medicineGenePhysicsBiochemistryThermodynamicsGeneticsAntibiotic Resistance in BacteriaVibrio bacteria research studiesInhalation and Respiratory Drug Delivery