INNATE IMMUNE EVASION MECHANISMS OF A HYPER- EPIDEMIC CLONE OF KLEBSIELLA PNEUMONIAE RESISTANT TO CARBEPENEMS

CASTILLO L; BIRNBERG WEISS F; MARTIRE GRECO D; BIGI, F; GOMEZ S.A.; LANDONI V.I; FERNÁNDEZ G C

Congreso; LXVI Reunion Anual de la Sociedad Argentina de Inmunologia; 2018

SAI

The emergence and rapid dissemination of Klebsiella pneumoniae (Kpn) carbapenem resistant has become a relevant problem in health care units, because it has been associated with higher mortality in susceptible patients, mainly attributed to Kpn Carbapenemase (KPC), an enzyme that hydrolyze carbapenems, one of the last resources in antibiotic treatment. As Kpn-KPC producers have been successful in terms of dissemination and persistence, we ask if Kpn-KPC could express mechanisms to avoid the innate immune response, focusing on their interaction with neutrophils (PMN). In this sense, we evaluated if one local isolate of Kpn-KPC, sequence type 258 (a hyper-epidemic clone), induces a differential response in healthy human isolated PMN, compared to another opportunistic pathogen as Eschericia coli ATCC 25922 (Eco). After evaluating some parameters of PMN activation, no differences were observed in the up-regulation of CD11b expression. However, reactive oxygen species (ROS) generation, measured by flow cytometry using dihidrorhodamine-123 (DHR) was lower for Kpn-KPC (ROS, % DHR+ PMN: Kpn-KPC=5.2±0.1; Eco=39.8±11.2, p