Candida is a type of fungus that is resident in our skin and vagina.Normally, it does not harm the human body, but when the homeostasis of the immune system and bacterial flora is disturbed by administration of anticancer drugs, antibacterial drugs, steroids, etc., it changes to a highly pathogenic state and begins to proliferate, and the oral cavity begins to grow. May cause a rash with persistent pain and itching in the mucous membranes, external auditory canal, genital area, and between the fingers and toes.However, it has not been known at all until now what causes these unpleasant emotions by "what components stimulate what receptors in which cells" of Candida.
Research groups such as Osaka University and the National Institute for Physiological Sciences of the National Institute of Natural Sciences have found that CSBG, a type of polysaccharide that is a component of Candida, stimulates epithelial cells in the skin to produce adenosine triphosphate (ATP) -secreting granules. It promoted release, and as a result, it was revealed that this ATP stimulated peripheral nociceptive nerves, causing pain and itching.
ATP is an important substance as an energy source for cells, and it is known that it is stocked in the cytoplasm in the form of secretory granules by the action of a molecule called a follicular nucleotide transporter (VNUT).Therefore, when a therapeutic drug having a VNUT inhibitory effect was administered to mice, the pain and itch caused by CSBG were significantly improved.From this, it was found that VNUT is an ideal therapeutic target for taking the symptoms associated with fungi.
This report not only clarified the whole picture of the onset mechanism of pain associated with fungal infection for the first time in the world, but also succeeded in finding a therapeutic target at the same time.These findings are important discoveries that contribute to the creation of a new interdisciplinary field that can be called "sensory immunology."
Paper information:[IScience] he ATP transporter VNUT mediates induction of Dectin-1-triggered Candida nociception.
