Bacterial host response articles from across Nature Portfolio

Faecal microbiome transplant has been shown to be able to reduce Clostridioides difficile infection. Here the authors show that an intestinal commensal protozoan reduces C. difficile infection by inhibiting neutrophil recruitment and affecting arginine-ornithine metabolism.

Upon pathogen attack, plants can trigger the “cry for help” response and assemble beneficial rhizobacteria. Here, the authors use nonpathogenic Pseudomonas syringae DC3000 derivatives to elicit a similar “cry for help” response as the wild-type pathogenic DC3000 in Arabidopsis.

Authors present a comparative immunological characterisation of Chlamydia vaccine, CTH522/CAF®01, in mice and humans. Findings suggest the mouse to be a good predictor of human immunity to the Chlamydia vaccine CTH522/CAF®01, and long-lasting protection in the mouse further supports the development of this promising vaccine candidate.

This study reports a mechanism whereby a Staphylococcus aureus protease induces itch by activating a host receptor on sensory neurons in the skin.

A recent study from Nature Communications reveals that Mycobacterium tuberculosis can hijack epigenetic machinery in host cells and induce host cell ferroptosis, which promotes pathogen pathogenicity and spread. These findings also suggest new therapeutic strategies to treat tuberculosis.

Commensal bacteria in the gut and their metabolites modulate the tonus of cancer immunosurveillance. Mao, Huang et al. demonstrate that the anticancer effects of caloric restriction depend on the expansion of acetate-producing immunostimulatory Bifidobacterium bifidum.

Gut commensal bacteria and their metabolites can contribute to metabolic diseases. Qiao, Liu et al. reveal that expansion of Parabacteroides merdae attenuates experimental atherosclerosis.

A study in germ-free mice shows that the gut microbiota can influence dietary choices of the host.

This study shows that staphylococcal superantigen induces macrophage dysfunction through interferon-γ, thus contributing to bacterial pathogenesis.