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PLoS One. 2010 Apr 7;5(4):e10033. doi: 10.1371/journal.pone.0010033.

Dissection of host cell signal transduction during Acinetobacter baumannii-triggered inflammatory response.

Author information

1
Program Infection and Immunity, Fundació Caubet-CIMERA Illes Balears, Bunyola, Spain.

Abstract

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.

PMID:
20383325
PMCID:
PMC2850920
DOI:
10.1371/journal.pone.0010033
[Indexed for MEDLINE]
Free PMC Article

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