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Bogza, A.

Publications and source records attributed to Bogza, A..

2 recordsLinked to original sources

The Salmonella phage shock protein system is required for defense against host antimicrobial peptides

Macrophages are professional phagocytes that play a major role in engulfing and eliminating invading pathogens. Some intracellular pathogens, such as Salmonella enterica serovar Typhimurium, exploit macrophages as niches for their replication, which requires precise and dynamic modulation of bacterial gene expression in order to resist the hostile intracellular environment. Here, we present a comprehensive analysis of the global transcriptome of S. Typhimurium across four stages of infection of primary macrophages. Our results revealed a profound change in early-stage gene expression dominated by pathways linked to metabolic processes required for Salmonella adaptation to the proinflammatory conditions of the macrophage. We identified the phage shock protein (Psp) system to be highly expressed in intracellular S. Typhimurium, with sustained high expression over the course of infection. We determined that the Psp system is regulated by the virulence-associated two-component system SsrA-SsrB, which coordinates its expression with critical bacterial functions required for immune evasion and intracellular survival. Functional assays demonstrated that the Psp system mediates resistance to host antimicrobial peptides, including cathelicidin-related antimicrobial peptide (CRAMP), which we demonstrate supports bacterial persistence in host tissues and survival within macrophages. Our findings establish the Psp system as a new and critical adaptive mechanism for evading host immune defenses and highlight the utility of temporal transcriptomics in unraveling the genetic strategies employed by S. Typhimurium during macrophage infection. Author summarySalmonella enterica is an important global pathogen that infects a wide range of mammalian hosts, requiring it to survive in diverse and hostile environments. A key aspect of Salmonella pathogenesis is its ability to reside within host immune cells like macrophages, where it must rapidly adapt to intracellular conditions. To do so, the bacteria must ensure correct spatiotemporal expression of virulence genes to maximise fitness in each environment. To better understand how Salmonella modulates its gene expression during infection of host cells, we defined its transcriptome at four distinct stages of primary murine macrophage infection. Our findings reveal that the first stage of early infection is dominated by changes in gene expression of metabolic circuits. Furthermore, we identified the phage-shock protein (Psp) system as highly expressed within intracellular Salmonella throughout the course of infection as a result of regulatory evolution that coordinates its expression with virulence genes. We showed that this system is required for bacterial survival within macrophages and host tissues by mediating resistance to host cationic antimicrobial peptides. These findings highlight the dynamic nature of Salmonellas transcriptional response during macrophage infection and uncover a previously unknown function of the Psp system as an adaptive mechanism for evading host immune defenses.

microbiology↗

A type 1 immune-stromal cell network mediates disease tolerance and barrier protection against intestinal infection

Type 1 immunity mediates host defense through pathogen elimination, but whether this pathway also impacts tissue function is unknown. Here we demonstrate that rapid induction of IFN{gamma} signaling coordinates a multi-cellular response that is critical to limit tissue damage and maintain gut motility following infection of mice with a tissue-invasive helminth. IFN{gamma} production is initiated by antigen-independent activation of lamina propria CD8+ T cells following MyD88-dependent recognition of the microbiota during helminth-induced barrier invasion. IFN{gamma} acted directly on intestinal stromal cells to recruit neutrophils that limited parasite-induced tissue injury. IFN{gamma} sensing also limited the expansion of smooth muscle actin-expressing cells to prevent pathological gut dysmotility. Importantly, this tissue-protective response had limited impact on parasite burden, indicating that IFN{gamma} supports a disease tolerance defense strategy. Our results have important implications for managing the pathophysiological sequelae of post-infectious gut dysfunction and chronic inflammatory diseases associated with stromal remodelling. HIGHLIGHTSO_LIType 1 immunity is required for disease tolerance to tissue-invasive infection. C_LIO_LIGut-resident CD8+ T cells produce IFN{gamma} in an antigen-independent, yet microbiota-dependent manner. C_LIO_LIIFN{gamma} signaling recruits neutrophils in a cell-extrinsic manner to limit helminth-induced tissue injury. C_LIO_LIDirect sensing of IFN{gamma} by intestinal stroma is essential to limit tissue damage and maintain gut motility during infection. C_LI

immunology↗