AsianScientist (July 11, 2017) – Scientists at the Immunology Frontier Research Center (IFReC) in Osaka, Japan, have discovered that pain neurons expressing the Nav1.8 ion channel inhibit fungal inflammation and bone destruction. The results of their study are published in Cell Reports.
Pain neurons exaggerate the inflammation phase of contact dermatitis and psoriasis. The Nav1.8 ion channel is a sodium ion channel subunit known to be expressed by neurons involved in the sensation of pain. Despite the importance of pain neurons in allergic and autoimmune inflammation, it is not known so far whether pain neurons modulate pathogen-induced inflammation.
Intriguingly, pain neurons that express the Nav1.8 ion channel also express Dectin-1, a β-glucan receptor. β-glucan is a polysaccharide produced by fungi such as Candida albicans. Dectin-1-mediated inflammation is potently suppressed by pain neurons, whereas bacteria-induced inflammation was unaffected. These observations suggested that pain neurons expressing the Nav1.8 ion channel specifically dampen the inflammatory response to fungal infection.
“We generated mice that lack the Nav1.8 ion channel-expressing pain neuron. After C. albicans or C. albicans derived β-glucan injection into the hind paw, these mice showed significantly increased footpad swelling and bone destruction,” said Assistant Professor Kenta Maruyama of the IFReC.
The researchers also found that Dectin-1-stumulated pain neurons produce robust amounts of calcitonin gene-related peptide, a neuropeptide that inhibits the activity of cells that break down bone. This means that pain neurons help prevent bone loss during fungal infection.
“Previous reports suggested that pain neurons are deleterious for inflammation, but our findings suggest that pain neurons may function primarily in suppressing fungal inflammation, rather than bacterial inflammation,” said Maruyama.
“Congenital insensitivity to pain with anhidrosis is an extremely rare hereditary disease characterized by impairment of nociceptor development. Manifestations of this disease are recurrent episodes of skin injury, osteomyelitis, bony fractures, and oral osteolysis. Our discovery may improve the therapeutic strategies of this disease and precise microbiological observation of this patient may clarify the bona-fide role of human pain neurons in fungal infection.”
The article can be found at: Maruyama et al. (2017) Nociceptors Boost the Resolution of Fungal Osteoinflammation via the TRP Channel-CGRP-Jdp2 Axis.
Source: Osaka University.
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