Mucin acts as a nutrient source and a signal for the differential expression of genes coding for cellular processes and virulence factors in Acinetobacter baumannii

Abstract

The capacity of Acinetobacter baumannii to persist and cause infections depends on its interaction with abiotic and biotic surfaces, including those found on medical devices and host mucosal surfaces. However, the extracellular stimuli affecting these interactions are poorly understood. Based on our previous observations, we hypothesized that mucin, a glycoprotein secreted by lung epithelial cells, particularly during respiratory infections, significantly alters A. baumannii’s physiology and its interaction with the surrounding environment. Biofilm, virulence and growth assays showed that mucin enhances the interaction of A. baumannii ATCC 19606T with abiotic and biotic surfaces and its cytolytic activity against epithelial cells while serving as a nutrient source. The global effect of mucin on the physiology and virulence of this pathogen is supported by RNA-Seq data showing that its presence in a low nutrient medium results in the differential transcription of 427 predicted protein-coding genes. The reduced expression of ion acquisition genes and the increased transcription of genes coding for energy production together with the detection of mucin degradation indicate that this host glycoprotein is a nutrient source. The increased expression of genes coding for adherence and biofilm biogenesis on abiotic and biotic surfaces, the degradation of phenylacetic acid and the production of an active type VI secretion system further supports the role mucin plays in virulence. Taken together, our observations indicate that A. baumannii recognizes mucin as an environmental signal, which triggers a response cascade that allows this pathogen to acquire critical nutrients and promotes host-pathogen interactions that play a role in the pathogenesis of bacterial infections.

Interspecies DNA acquisition by a naturally competentAcinetobacter baumanniistrain

“…The acquisition of bla OXA-23 but not of bla KPC suggests that A. baumannii may have a preferential affinity to acquire and maintain certain carbapenemases over other. The observed results agree with the observation that bla OXA-like enzymes are frequently found in this species and only a few reports of bla KPC A. baumannii positive isolates were reported in the literature (41, 42). The intl2 gene together with the typical gene cassette array of the class 2 integron In2-7, dfrA1-sat2-aadA1-orfX-ybfA-ybfB-ybgA , was found.…”

“…To test the role of bacterial predation in A. baumannii the ability of A118 to lyse K. pneumoniae , as well as E. coli was assessed by performing killing assays. A118 was used as predator and VA360 or E. coli MG1655-Rif as preys as previously described (41, 42). We clearly observed that A118 kills VA360 (Fig.…”

A Light-Regulated Type I Pilus Contributes to Acinetobacter baumannii Biofilm, Motility, and Virulence Functions

“…Infection of polarized A549 human alveolar epithelial cells. A549 cells were polarized and infected with bacteria cultured in LB broth as described previously (45), using 10 6 bacteria/ml, and incubated for 48 h at 37°C in the presence of 5% CO 2 . All polarized cell samples were fixed after 48 h of infection and analyzed by SEM as described previously (44).…”

Human serum albumin alters specific genes that can play a role in survival and persistence in Acinetobacter baumannii

“…These factors can contribute to the pathogen’s overall survival against host immune effectors, however, these are not the only strategies the microbe may use to promote persistence. The persistence state is an evolutionarily adaptive strategy indicated by a change in metabolic profile, latent growth patterns, and has been associated with expression of toxin/antitoxin systems 11 , 12 . Persistence phenotypes are environmentally modulated, therefore, it is important to address changes in bacterial physiology under stress 13 .…”