Stenotrophomonas maltophilia is a gram-negative, multidrug-resistant, opportunistic human pathogen responsible for hard-to-treat infections in immunocompromised individuals. Besides being recognized as an important clinical pathogen, S. maltophilia is also widespread in the natural environment, with knowledge of the pathogenic potential of the environmental S. maltophilia pool still lacking. In this study, we aimed to identify the differences in virulence-related traits between clinical and environmental S. maltophilia isolates by assessing their genotypic and phenotypic features. For this purpose, 40 S. maltophilia isolates from natural environment and 34 clinical isolates obtained from patients were analysed. We observed a high degree of genotypic diversity among the isolates irrespective of their origin. Although antibiotic resistance- and virulence-related genes were more prevalent in the clinical isolates, the majority of the analysed genes were also present in the environmental isolates. Most importantly, the phenotypic features, specifically the ability to form biofilms and display twitching motility at human body temperature were predominantly characteristic to the clinical isolates. Our study indicates that adaptation to endure human body temperature is a feature strongly linked to S. maltophilia strains of clinical origin, and is significant when differentiating harmless environmental bacteria from pathogenic S. maltophilia isolates.

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 and Stenotrophomonas maltophilia are opportunistic pathogens causing hospital infections with limited treatment options due to bacterial multidrug resistance. Here, we report that antimicrobial photodynamic therapy (aPDT) based on the natural photosensitizers riboflavin and chlorophyllin inactivates A. baumannii and S. maltophilia. The riboflavin and chlorophyllin photostability experiments assessed the photomodifications of photosensitizers under the conditions subsequently used to inactivate A. baumannii and S. maltophilia. A. baumannii planktonic cells were more sensitive to riboflavin-aPDT, while biofilm bacteria were more efficiently inactivated by chlorophyllin-aPDT. S. maltophilia planktonic and biofilm cells were more susceptible to chlorophyllin-aPDT compared to riboflavin-aPDT. The results suggest that riboflavin- and chlorophyllin-aPDT can be considered as a potential antimicrobial treatment for A. baumannii and S. maltophilia inactivation.

Publications addressing air pollution-induced human respiratory microbiome shifts are reviewed in this article. The healthy respiratory microbiota is characterized by a low density of bacteria, fun... Plain language summary The community of bacteria, viruses and fungi in the human body, known as the microbiome, plays an important role in human health. These communities vary in different location...

As one of the most diverse habitats of microorganisms, soil has been recognised as a reservoir of both antibiotics and the antibiotic resistance genes (ARGs). Bacteria naturally inhabiting soil or water often possess innate ARGs to counteract the chemical compounds produced by competitors living in the same environment. When such bacteria are able to cause infections in immunocompromised patients, their strong innate antibiotic resistance mechanisms make treatment difficult. We generated functional gene libraries using antibiotic-resistant Stenotrophomonas maltophilia and Chryseobacterium spp. bacteria isolated from agricultural soils in Lithuania to select for the genetic determinants responsible for their resistance. We were able to find novel variants of aminoglycoside and β-lactam resistance genes, with β-lactamases isolated from the Chryseobacterium spp. functional gene library, one of which is a variant of IND-like metallo-β-lactamase (MBL) IND-17 and the other of which is a previously uncharacterised MBL we named CHM (Chryseobacterium metallo β-lactamase). Our results indicate that soil microorganisms possess a diversity of ARG variants, which could potentially be transferred to the clinical setting.

Blood vessels in different vascular beds vary in size, which is essential for their function and fluid flow along the vascular network. Molecular mechanisms involved in the formation of a vascular lumen of appropriate size, or tubulogenesis, are still only partially understood.Src homology 2 domain containing E (She)protein was previously identified in a screen for proteins that interact with Abelson (Abl)-kinase. However, its biological role has remained unknown. Here we demonstrate that She and Abl signaling regulate vessel size in zebrafish embryos and human endothelial cell culture. Zebrafishshemutants displayed increased endothelial cell number and enlarged lumen size of the dorsal aorta (DA) and defects in blood flow, eventually leading to the DA collapse. Vascular endothelial specific overexpression ofsheresulted in a reduced diameter of the DA, which correlated with the reduced arterial cell number and lower endothelial cell proliferation. Chemical inhibition of Abl signaling in zebrafish embryos caused a similar reduction in the DA diameter and alleviated theshemutant phenotype, suggesting that She acts as a negative regulator of Abl signaling. Enlargement of the DA size inshemutants correlated with an increased endothelial expression ofclaudin 5a (cldn5a), which encodes a protein enriched in tight junctions. Inhibition ofcldn5aexpression partially rescued the enlarged DA inshemutants, suggesting that She regulates DA size, in part, by promotingcldn5aexpression. SHE knockdown in human endothelial umbilical vein cells resulted in a similar increase in the diameter of vascular tubes, and also increased phosphorylation of a known ABL downstream effector CRKL. These results argue that SHE functions as an evolutionarily conserved inhibitor of ABL signaling and regulates vessel and lumen size during vascular tubulogenesis.