名古屋大学 · 医学
Keiko Kataoka教授の研究室は、腸内微生物と宿主の免疫系の相互作用が健康と疾患に与える影響を解明する腸内マイクロバイオームと免疫調節の研究を主軸としています。特に、炎症性腸疾患や自己免疫疾患、眼疾患における腸-免疫-臓器軸のメカニズムに注目し、微生物代謝産物やβグルカンが免疫応答に与える影響を分子レベルで解明しています。また、網膜剥離に伴う炎症小体の活性化や新生血管形成のメカニズムについても、臨床的意義を踏まえた基礎研究を展開しています。
Figures are computed from collected data and may differ slightly.
The role of the intestinal microbiota in human health is gaining more attention since clear changes in the composition of the intestinal bacteria or environment are seen in patients with inflammatory bowel disease, allergy, autoimmune disease, and some lifestyle-related illnesses. A healthy gut environment is regulated by the exquisite balance of intestinal microbiota, metabolites, and the host's immune system. Imbalance of these factors in genetically susceptible persons may promote a disease s
Although (1-->3)-beta-d-glucans, which are one of major fungal cell wall components, are known to activate invertebrate innate immune systems, their activities on mammalian cells remain elusive. Here, we report their activities on mouse macrophages. Among the various (1-->3)-beta-d-glucans, curdlan, a linear (1-->3)-beta-d-glucan, although not branched beta-glucans, exhibits significant activity to stimulate nuclear factor-kappaB in macrophages. The activity of curdlan is dramatically enhanced b
Vitreal macrophages are attracted to the site of pathologic angiogenesis triggered by retinal ischemia, where they actively participate in vascular development.
Detachment of photoreceptors from the retinal pigment epithelium is seen in various retinal disorders, resulting in photoreceptor death and subsequent vision loss. Cell death results in the release of endogenous molecules that activate molecular platforms containing caspase-1, termed inflammasomes. Inflammasome activation in retinal diseases has been reported in some cases to be protective and in others to be detrimental, causing neuronal cell death. Moreover, the cellular source of inflammasome
OCTA revealed that the vessel junction densities of type 1 CNVs were lower than those of type 2 CNVs, suggesting type 1 CNV vessels are more mature than type 2 CNV vessels.
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