Nagoya University · Medicine
Professor Keiko Kataoka's research lab focuses on the immunological and cellular mechanisms underlying retinal diseases, with a particular emphasis on the role of innate immunity, inflammasomes, and macrophage function in retinal pathologies such as retinal detachment and choroidal neovascularization. The lab investigates how microbial metabolites and fungal components like (1-->3)-beta-d-glucans modulate immune responses, especially in macrophages, and explores the interplay between the microbiota, host immunity, and tissue homeostasis. Using advanced imaging techniques such as OCTA, the lab examines vascular remodeling and maturation in pathological conditions, aiming to uncover therapeutic targets for vision-threatening diseases.
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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