Stenotrophomonas maltophilia is a ubiquitous environmental bacterium that has recently emerged as a multidrug-resistant opportunistic pathogen causing bloodstream, respiratory, and urinary tract infections. The connection between the commensal environmental S. maltophilia and the opportunistic pathogen strains is still under investigation. Bacterial toxin–antitoxin (TA) systems have been previously associated with pathogenic traits, such as biofilm formation and resistance to antibiotics, which are important in clinical settings. The same species of the bacterium can possess various sets of TAs, possibly influencing their overall stress response. While the TA systems of other important opportunistic pathogens have been researched, nothing is known about the TA systems of S. maltophilia. Here, we report the identification and characterization of S. maltophilia type II TA systems and their prevalence in the isolates of clinical and environmental origins. We found 49 putative TA systems by bioinformatic analysis in S. maltophilia genomes. Despite their even spread in sequenced S. maltophilia genomes, we observed that relBE, hicAB, and previously undescribed COG3832-ArsR operons were present solely in clinical S. maltophilia isolates collected in Lithuania, while hipBA was more frequent in the environmental ones. The kill-rescue experiments in Escherichia coli proved higBA, hicAB, and relBE systems to be functional TA modules. Together with different TA profiles, the clinical S. maltophilia isolates exhibited stronger biofilm formation, increased antibiotic, and serum resistance compared to environmental isolates. Such tendencies suggest that certain TA systems could be used as indicators of virulence traits.

Acinetobacter baumannii is an opportunistic pathogen characterised by multidrug resistance and is among the leading causes of nosocomial infections. This study investigated the role of capsular polysaccharides (CPS) in antimicrobial resistance and host-pathogen interaction. CPS-deficient mutant (∆ galU ) displayed increased susceptibility to gentamicin, tetracycline, colistin, and sodium dodecyl sulfate (SDS). In the absence of CPS, bacteria adapted by forming biofilm, characterised by a thicker extracellular matrix. These biofilms displayed increased resistance to colistin, chlorhexidine, and hydrogen peroxide, but remained sensitive to tetracycline and SDS. CPS were also essential for the resistance to photodynamic therapy induced by blue light and chlorophyllin. Gene expression analysis revealed upregulation of galU gene under the exposure to antibiotics, blue light, fetal bovine serum, and during the contact with macrophages. CPS-deficient mutant and its derived outer membrane vesicles elicited a stronger pro-inflammatory response, compared to wild-type. CPS shielding A. baumannii demonstrated the ability to induce caspase-3 activation to a greater extent compared to the mutant strain. Moreover, purified CPS induced pro-inflammatory cytokine expression in sterile infection and promoted neutrophil chemotaxis. Altogether, this study demonstrates that CPS not only mask A. baumannii virulence surface structures, but also actively modulate host immune response and antimicrobial resistance.