Abstract
Acinetobacter baumannii has emerged as a significant opportunistic Gram-negative pathogen and causative agent of nosocomial pneumonia especially in immunocompromised individuals in intensive care units. Recent advances to understand the contribution and function of A. baumannii virulence factors in its pathogenesis have begun to elucidate how this bacterium interacts with immune cells and its interesting mechanisms for multi-antibiotic resistance. Taking advantage of the availability of the A. baumannii AB5075 transposon mutant library, we investigated the impact of the A. baumannii Clp genes, which encode for a chaperone-protease responsible for the degradation of misfolded proteins, on bacterial virulence in a model of pneumonia using C57BL/6 mice and survival within J774.16 macrophage-like cells. Clp-protease A. baumannii mutants exhibit decreased virulence in rodents, high phagocytic cell-mediated killing and reduced biofilm formation. Capsular staining showed evidence of encapsulation in A. baumannii AB5075 and Clp-mutant strains. Surprisingly, clpA and clpS mutants displayed irregular cell morphology, which may be important in the biofilm structural deficiencies observed in these strains. Interestingly, clpA showed apical-like growth, proliferation normally observed in filamentous fungi. These findings provide new information regarding A. baumannii pathogenesis and may be important for the development of therapies intended at reducing morbidity and mortality associated with this remarkable pathogen.
Highlights
Acinetobacter baumannii is a Gram-negative coccobacillus, motile and biofilm-forming opportunistic pathogen [1]
A. baumannii causes a variety of hospital-related infections including ventilator-associated pneumonia and bloodstream, wound and urinary tract infections that can become complicated resulting in meningitis and osteomyelitis [1,2]
We found that the Clp chaperone-protease mutants demonstrated diminished virulence, lower survival within macrophages and less biofilm formation than wild-type A. baumannii AB5075
Summary
Acinetobacter baumannii is a Gram-negative coccobacillus, motile and biofilm-forming opportunistic pathogen [1]. In the past two decades, A. baumannii has emerged as a major worldwide burden in countries with developed healthcare systems because of its capacity to rapidly develop antibiotic resistance and persist in challenging environments [1,3]. A. baumannii strains impervious to carbapenems [4] and amikacin [5] have been frequently isolated from clinical specimens. Carbapenem-resistant A. baumannii strains were responsible for approximately. The ability of A. baumannii to attach to solid surfaces and form biofilms give the bacterium an advantage and ideal niche for its extended prevalence in hospital settings and in various hostile environments [1]
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