Autoinflammatory syndrome induced by the cold (or familial cold urticaria) is manifested by bouts of fever triggered by the cold, accompanied by hives attacks and digestive and joint pain. To date, around twenty patients have been identified, all carrying a mutation in a gene.
Until now, the pathophysiological mechanisms underlying the disease have remained unknown. A research team led by Mathias Chamaillard, Inserm researcher at the Lille Infection and Immunity Center has highlighted the implication in the occurrence of the disease of an exacerbated inflammatory response against intestinal flora.
The intestine becomes permeable when it is cold
The decrease in tolerance in subjects with autoinflammatory cold syndrome generates chronic inflammation which could explain the intestinal pain in patients. But why does the cold trigger additional manifestations outside the digestive system? Researchers suspect an increase in intestinal permeability in low temperature.
“In healthy subjects, this phenomenon would be of no consequence, but in sick subjects, many molecules with pro-inflammatory activity as well as bacterial debris could pass en masse into the blood” underline the researchers. A secondary local inflammation could therefore partly explain the other symptoms such as fever, headaches and joint pain.
The results of this study were published in Nature communications.
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