Abstract
Acinetobacter baumannii persists in the medical environment and causes severe human nosocomial infections. Previous studies showed that low-level ethanol exposure increases the virulence of A. baumannii ATCC 17978. To better understand the mechanisms involved in this response, 2-D gel electrophoresis combined with mass spectrometry was used to investigate differential protein production in bacteria cultured in the presence or absence of ethanol. This approach showed that the presence of ethanol significantly induces and represses the production of 22 and 12 proteins, respectively. Although over 25% of the ethanol-induced proteins were stress-response related, the overall bacterial viability was uncompromised when cultured under these conditions. Production of proteins involved in lipid and carbohydrate anabolism was increased in the presence of ethanol, a response that correlates with increased carbohydrate biofilm content, enhanced biofilm formation on abiotic surfaces and decrease bacterial motility on semi-solid surfaces. The presence of ethanol also induced the acidification of bacterial cultures and the production of indole-3-acetic acid (IAA), a ubiquitous plant hormone that signals bacterial stress-tolerance and promotes plant-bacteria interactions. These responses could be responsible for the significantly enhanced virulence of A. baumannii ATCC 17978 cells cultured in the presence of ethanol when tested with the Galleria mellonella experimental infection model. Taken together, these observations provide new insights into the effect of ethanol in bacterial virulence. This alcohol predisposes the human host to infections by A. baumannii and could favor the survival and adaptation of this pathogen to medical settings and adverse host environments.
Highlights
The Gram-negative aerobic coccobacillus Acinetobacter baumannii is recognized for its ability to cause severe nosocomial infections including pneumonia, urinary tract infections, wound and burn infections, secondary meningitis and systemic infections [1,2]
A. baumannii causes colonization more often than infection and preferentially resides in medical environments and devices [2,12,13,14]. This behavior could be due to its capacity to produce CsuA/BABCD-mediated pili [15] and the Bap protein [16], which are involved in biofilm formation; poly-ß-1-6-Nacetylglucosamine, which is critical for the formation of fully developed biofilms [17]; the outer membrane protein OmpA, which plays a role in bacteria-host interactions and cell apoptosis [18,19,20]; lipopolysaccharides, which are involved in host immune responses [21,22]; a phospholipase D, which is responsible for serum resistance [23]; K1 capsular polysaccharide, which acts as an efficient protectin in experimental animal infections [24]; and to express acinetobactin-mediated iron acquisition functions, which are involved in bacterial persistence, cell damage and killing of infected hosts [25]
Previous studies on effects of ethanol on the virulence of A. baumannii ATCC 17978 were performed using D. discoideum and C. elegans as hosts [33,34]. While these two experimental models provided valuable initial insights into the potential expression of A. baumannii functions involved in its interaction with complex microorganisms, these models may not reflect all the interactions between this pathogen and the human host. These considerations prompted us to test the role of ethanol in the virulence of A. baumannii ATCC 17978 using G. mellonella, an invertebrate host capable of mounting complex defense responses similar to those described in the human host [45]
Summary
The Gram-negative aerobic coccobacillus Acinetobacter baumannii is recognized for its ability to cause severe nosocomial infections including pneumonia, urinary tract infections, wound and burn infections, secondary meningitis and systemic infections [1,2]. A. baumannii causes colonization more often than infection and preferentially resides in medical environments and devices [2,12,13,14] This behavior could be due to its capacity to produce CsuA/BABCD-mediated pili [15] and the Bap protein [16], which are involved in biofilm formation; poly-ß-1-6-Nacetylglucosamine, which is critical for the formation of fully developed biofilms [17]; the outer membrane protein OmpA, which plays a role in bacteria-host interactions and cell apoptosis [18,19,20]; lipopolysaccharides, which are involved in host immune responses [21,22]; a phospholipase D, which is responsible for serum resistance [23]; K1 capsular polysaccharide, which acts as an efficient protectin in experimental animal infections [24]; and to express acinetobactin-mediated iron acquisition functions, which are involved in bacterial persistence, cell damage and killing of infected hosts [25]. This genome-wide analysis showed that besides inducing genes involved in its assimilation and utilization as a nutrient, ethanol controls the differential transcription of A. baumannii ATCC 17978 genes responsible for stress responses as well as the production of permeases, efflux pump proteins, a secreted phospholipase C, and proteins involved in phosphate and iron transport
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
