Key clinical message: IL-36 might play a role as an initial immune mechanism against chikungunya fever, and regulating IL-36 production could be a potential treatment approach for this condition.
Abstract: Two Japanese siblings visited Cook Islands in 2015 and developed Chikungunya fever upon their return. The sister experienced high fever, joint pain, and leg swelling, while the brother had joint pain and a rash. Both siblings had a confirmed CHIKV infection and continued to experience prolonged joint pain, with the sister enduring chronic pain for about a year. In this study, the levels of IL-36 in the serum of two siblings who were infected with chikungunya fever during the acute and recovery phases were compared using ELISA. IL-36 is a cytokine that induces inflammation and is produced by cells in tissues such as the skin and mucosa. It was hypothesized that IL-36 may be involved in persistent joint pain after chikungunya fever infection. Both siblings experienced long-lasting joint pain after chikungunya fever infection. The levels of IL-36α and IL-36β decreased by 56 days after infection. In the results, IL-36 plays an important role in host immunity and may act as part of the immune response during chikungunya virus infection. Inhibiting the release of IL-36 could be a promising approach for developing new treatment methods for chikungunya fever.
Keywords: IL‐36; IL‐36α; IL‐36β; chikungunya fever; immune defense; joint pain.
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