Innate Immune Responses to Acinetobacter baumannii in the Airway

Abstract

Acinetobacter baumannii is an emerging opportunistic pathogen that has risen to become a serious global threat, prevalent in health care settings and the community, which results in high morbidity and mortality rates. Its alarming expansion of antibiotic resistance is one of the most problematic traits of A. baumannii and as so, this bacterium has been classified as a serious threat and high priority target by the CDC. The most common types of infections induced by this pathogen include pneumonia (both hospital and community acquired), bacteremia, skin and soft tissue, urinary tract infections, endocarditis, and meningitis. Nosocomial pneumonia is the most prevalent of these. This review summarizes the current state of the signaling and innate immune components activated in response to A. baumannii infection in the airway.

Keywords: airway; host-pathogen; innate immunity; lung.

FIG. 1.

Innate immune responses to Acinetobacter baumannii in the airway. Epithelial cells are one of the first defenses encountered by A. baumannii. As a result of this interaction AMP that can effectively kill A. baumannii are produced. The NOD/RIP2 axis in epithelial cells contributes to the production of inflammatory cytokines as well as in the control of cell invasion and replication by A. baumannii. TLR receptor 4 and 9 have been shown to be important in bacterial clearance, whereas TLR2 inactivation has exhibited mixed results as far as bacterial clearance. Macrophage production of chemoattractants, namely MIP-2 and CXCL1/KC, contributes to neutrophil recruitment upon infection. Early recruitment of functional neutrophils is an essential step to kill and control A. baumannii proliferation. NET production and their role in response to A. baumannii are still inconclusive as there are conflicting results, but ROS production is essential for the ability of neutrophils to kill A. baumannii. The inflammasome is activated upon infection and although not important for clearance, excess levels of IL-1β contribute to immunopathology. AMP, antimicrobial peptide; NETS, neutrophil extracellular traps; ROS, reactive oxygen species; TLR, toll-like receptor.