Abstract

The RNA chaperone Hfq is involved in the riboregulation of diverse genes via small RNAs. Recent studies have demonstrated that Hfq contributes to the stress response and the virulence of several pathogens, and the roles of Hfq vary among bacterial species. Here, we attempted to elucidate the role of Hfq in Acinetobacter baumannii ATCC 17978. In the absence of hfq, A. baumannii exhibited retarded cell growth and was highly sensitive to environmental stress, including osmotic and oxidative pressure, pH, and temperature. Compared to the wild-type, the Hfq mutant had reduced outer membrane vesicles secretion and fimbriae production as visualized by atomic force microscopy. The absence of hfq reduced biofilm formation, airway epithelial cell adhesion and invasion, and survival in macrophage. Further, the hfq mutant induced significantly higher IL-8 levels in airway epithelial cells, which would promote bacterial clearance by the host. In addition to results similar to those reported for other bacteria, our findings demonstrate that Hfq is required in the regulation of the iron-acquisition system via downregulating the bauA and basD genes, the stress-related outer membrane proteins carO, A1S_0820, ompA, and nlpE, and the stress-related cytosolic proteins uspA and groEL. Our data indicate that Hfq plays a critical role in environmental adaptation and virulence in A. baumannii by modulating stress responses, surface architectures, and virulence factors. This study is the first to illustrate the functional role of Hfq in A. baumannii.

Highlights

  • Acinetobacter baumannii has emerged recently as a major cause of healthcare-associated infections worldwide (Maragakis and Perl, 2008)

  • We demonstrated that loss of hfq affects a number of virulence-associated phenotypes, including bacterial morphology, biofilm formation, resistance to stress response, cell adhesion, and invasion ability, in A. baumannii ATCC17978

  • We studied the effects of an Hfq-like protein on the pathogenesis of A. baumannii ATCC 17978

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Summary

Introduction

Acinetobacter baumannii has emerged recently as a major cause of healthcare-associated infections worldwide (Maragakis and Perl, 2008). These organisms have been implicated in a diverse range of infections in hospitalized patients, especially patients with prolonged stays in intensive care units (Consales et al, 2011). The remarkable resistance phenotype may be facilitated by the ability of A. baumannii strains, those isolated from catheter-related urinary or bloodstream infections, to form biofilms that adhere to and persist on abiotic surfaces (Lee et al, 2008). The ability of A. baumannii to adhere to a number of epithelial cell lines has recently been investigated (Lee et al, 2006; Giannouli et al, 2013). A number of novel genes in A. baumannii with significant roles in pathogenesis have been discovered (Smith et al, 2007; Vallenet et al, 2008), the intrinsic regulatory mechanisms involved in environmental adaptation and disease progression remain unclear

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