bioRxiv Science⌕ Search

Biology subjects

Antelo-Varela, M.

Publications and source records attributed to Antelo-Varela, M..

3 recordsLinked to original sources

Subpopulations of Pseudomonas aeruginosa inflict distinct tissue damage during infection

P. aeruginosa is a Gram-negative, ubiquitous, opportunistic pathogen that can colonize open wounds and the respiratory airways and is particularly problematic for patients suffering from cystic fibrosis (CF) where it can cause chronic infections. One factor contributing to P. aeruginosa diversity during infection is phenotypic heterogeneity. Phenotypic heterogeneity is the ability of bacteria to express different levels of selected pathways, giving rise to multiple bacterial subpopulations in the same environment. The prevalence and relevance of this phenomenon have been poorly characterized in infection models. In this study, we developed strategies to detect these subpopulations via single cell reporters, flow cytometry and fluorescence microscopy, in simple infection models and a physiologically relevant, transwell-based model of the bronchial epithelium. Next, we optimized cell sorting coupled to low input proteomics approaches to characterize the physiological state of the identified subpopulations, and genetically manipulated P. aeruginosa to lock them in ON or OFF states of expression of phenotypically heterogeneous pathways. We identify that type IVc/Tad pili are expressed in a subset of P. aeruginosa cells and inflict damage to the host tissue, while type Tad pili-negative subpopulations express other virulence factors instead. Lastly, we validated the heterogeneous expression of this machinery across clinical strains. Our findings uncovered the diversity of strategies employed by P. aeruginosa for pathogenesis, where distinct bacterial subpopulations use different virulence factors to damage respiratory epithelia.

microbiology↗

Pervasive bacterial and prophage hybridization during chronic gut inflammation

Inflammatory bowel diseases (IBD) are modulated by microbiota composition, host genetics, and environmental factors1. Humans and other mammals are colonized by multiple strains of Escherichia coli, a species that expands in abundance in IBD patients2. The state of chronic inflammation characteristic of IBD is expected to intensify selective pressures on the gut microbial community, leading to distinct adaptive trajectories among its constituents. Here we couple in vivo experimental evolution with short- and long-read sequencing to test this hypothesis at the level of mutation and horizontal gene transfer (HGT). By colonizing IL10KO mice, a model of IBD3, and healthy wild-type mice with two strains of E. coli, we show that the tempo and mode of evolution are strain-specific and strongly shaped by host inflammatory status. Unique mutations associate with host inflammatory status independently of microbiota composition, and rates of transfer are diagnostic of chronic inflammation. Extensive transduction events occur in the inflamed gut, giving rise to hybrid clones that form a new genetic lineage, one that becomes dominant in this disease context. The high levels of recombination between prophages uncovered here point to a critical role of HGT and viral evolution in IBD.

microbiology↗

Mechanisms of P. aeruginosa resistance to Type VI Secretion System attacks

The Type VI Secretion System (T6SS) is a molecular nanomachine that injects toxic effector proteins into the environment or neighbouring cells, playing an important role in interbacterial competition and host antagonism during infection. Pseudomonas aeruginosa encodes three T6SSs. The H1-T6SS delivers toxins in response to attacks mediated by the T6SS of aggressive bacteria, suggesting that P. aeruginosa can resist T6SS assaults. The mechanisms of resistance are poorly characterized. Here, we performed a CRISPRi screen to identify pathways involved in resistance to T6SS effectors of Acinetobacter baylyi and Vibrio cholerae. We show that members of the GacA/GacS regulon, such as the mag operon or aas, and GacA-independent factors, such as the outer membrane protein OprF, confer resistance to different types of T6SS toxins. Interestingly, some of these T6SS resistance mechanisms lead to higher antibiotic susceptibility, suggesting complex evolutionary links between T6SS and antibiotic resistance.

microbiology↗