Publications by authors named "N Inohara"

Staphylococcus aureus can cause outbreaks and becomes multi-drug resistant through gene mutations and acquiring resistance genes. However, why S. aureus easily adapts to hospital environments, promoting resistance and recurrent infections, remains unknown.

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The ectopic gut colonization by orally derived pathobionts has been implicated in the pathogenesis of various gastrointestinal diseases, including inflammatory bowel disease (IBD). For example, gut colonization by orally derived spp. has been linked to IBD in mice and humans.

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The gut microbiota promotes immune system development in early life, but the interactions between the gut metabolome and immune cells in the neonatal gut remain largely undefined. Here, we demonstrate that the neonatal gut is uniquely enriched with neurotransmitters, including serotonin, and that specific gut bacteria directly produce serotonin while down-regulating monoamine oxidase A to limit serotonin breakdown. We found that serotonin directly signals to T cells to increase intracellular indole-3-acetaldehdye and inhibit mTOR activation, thereby promoting the differentiation of regulatory T cells, both ex vivo and in vivo in the neonatal intestine.

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Article Synopsis
  • - Immune checkpoint inhibitors can boost antitumor immunity but may cause immune-related adverse events (irAEs), with colitis being a significant and severe issue that can lead to stopping treatment.
  • - Traditional laboratory mice do not exhibit strong colitis with these treatments, but research shows that mice with wild-caught microbiota can develop noticeable colitis when treated with anti-CTLA-4 antibodies.
  • - The study found that colitis results from aggressive activation of certain immune cells and suggests using modified anti-CTLA-4 nanobodies that avoid colitis while still enhancing antitumor effects.
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