Dissection of host cell signal transduction during Acinetobacter baumannii-triggered inflammatory response.
Infected airway epithelial cells up-regulate the expression of chemokines, chiefly IL-8, and antimicrobial molecules including beta-defensins (BD). Acinetobacter baumannii is a cause of hospital-acquired pneumonia. We examined whether A. baumannii induced the expressions of IL-8 and BD2 by airway epithelial cells and the receptors implicated in bacterial detection. A549 and human primary airway cells released IL-8 upon infection. A. baumannii-infected cells also increased the expression of BD2 which killed A. baummannii strains. IL-8 induction was via NF-kappaB and mitogen-activated kinases p38 and p44/42-dependent pathways. A. baumannii engaged Toll-like receptor (TLR) 2 and TLR4 pathways and A549 cells could use soluble CD14 as TLRs co-receptor. A. baumannii lipopolysaccharide stimulated IL-8 release by A549 cells and sCD14 facilitated the recognition of the lipopolysaccharide. Mass spectrometry analysis revealed that A. baumannii lipid A structure matches those with endotoxic potential. These results demonstrate that airway epithelial cells produce mediators important for A. baumannii clearance.
March
Catalina
C
Program Infection and Immunity, Fundació Caubet-CIMERA Illes Balears, Bunyola, Spain.
Regueiro
Verónica
V
Llobet
Enrique
E
Moranta
David
D
Morey
Pau
P
Garmendia
Junkal
J
Bengoechea
José A
JA
D000151:Acinetobacter Infections; D040981:Acinetobacter baumannii / Q000276:immunology*; D002460:Cell Line; D004847:Epithelial Cells; D054884:Host-Pathogen Interactions; D006801:Humans; D007249:Inflammation / Q000209:etiology*; D018836:Inflammation Mediators / Q000032:analysis; D016209:Interleukin-8 / Q000235:genetics; D011014:Pneumonia / Q000276:immunology / Q000382:microbiology*; D012137:Respiratory System / Q000166:cytology; D015398:Signal Transduction; D015854:Up-Regulation / Q000235:genetics; D023083:beta-Defensins / Q000235:genetics
D018836:Inflammation Mediators; D016209:Interleukin-8; D023083:beta-Defensins
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