Keio University · Biochemistry, Genetics and Molecular Biology
Professor Kenya Honda's research lab focuses on host-microbiota interactions, particularly the immunological and metabolic impacts of commensal and ectopically colonizing bacteria, such as *Klebsiella* spp. from the oral microbiota, on intestinal immunity and inflammatory diseases. The lab investigates innate immune sensing mechanisms, especially Toll-like receptor (TLR)-mediated signaling pathways involving MyD88, IRF-7, and type I interferons (IFN-α/β), to understand how microbial signals are translated into immune responses. A central theme is the role of the microbiome in shaping mucosal immunity and disease susceptibility, with a strong emphasis on gnotobiotic models and molecular immunology. The lab also explores the complex crosstalk between viral sensing pathways (e.g., TLR3, PKR) and type I interferon signaling in dendritic cell maturation and immune regulation.
Figures are computed from collected data and may differ slightly.
Intestinal colonization by bacteria of oral origin has been correlated with several negative health outcomes, including inflammatory bowel disease. However, a causal role of oral bacteria ectopically colonizing the intestine remains unclear. Using gnotobiotic techniques, we show that strains of <i>Klebsiella</i> spp. isolated from the salivary microbiota are strong inducers of T helper 1 (T<sub>H</sub>1) cells when they colonize in the gut. These <i>Klebsiella</i> strains are resistant to multip
The mammalian alimentary tract harbors hundreds of species of commensal microorganisms (microbiota) that intimately interact with the host and provide it with genetic, metabolic, and immunological attributes. Recent reports have indicated that the microbiota composition and its collective genomes (microbiome) are major factors in predetermining the type and robustness of mucosal immune responses. In this review, we discuss the recent advances in our understanding of host-microbiota interactions
Toll-like receptor (TLR) activation is central to immunity, wherein the activation of the TLR9 subfamily members TLR9 and TLR7 results in the robust induction of type I IFNs (IFN-alpha/beta) by means of the MyD88 adaptor protein. However, it remains unknown how the TLR signal "input" can be processed through MyD88 to "output" the induction of the IFN genes. Here, we demonstrate that the transcription factor IRF-7 interacts with MyD88 to form a complex in the cytoplasm. We provide evidence that t
A complex mechanism may be operational for dendritic cell (DC) maturation, wherein Toll-like receptor and other signaling pathways may be coordinated differently depending on the nature of the pathogens, in order for DC maturation to be most effective to a given threat. Here, we show that IFN-alpha/beta signaling is selectively required for the maturation of DCs induced by double-stranded RNA or viral infection in vitro. Interestingly, the maturation is still observed in the absence of either of
The type I IFN-alpha/beta gene family was identified about a quarter of a century ago as a prototype of many cytokine gene families, which led to the subsequent burst of studies on molecular mechanisms underlying cytokine gene expression and signaling. Although originally discovered for their activity to confer an antiviral state on cells, more evidence has recently been emerging regarding IFN-alpha/beta actions on cell growth, differentiation and many immunoregulatory activities, which are of e
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