biostudies-literaturede Araujo SFundação de Amparo à Pesquisa do Estado de Minas GeraisConselho Nacional de Desenvolvimento Científico e TecnológicoMedical Research CouncilL'Oréal-UNESCO-ABC2717https://www.ebi.ac.uk/biostudies/studies/S-EPMC9454528biostudies-literatureUnknown11(17)Chikungunya (CHIKV) is an arthritogenic alphavirus that causes a self-limiting disease usually accompanied by joint pain and/or polyarthralgia with disabling characteristics. Immune responses developed during the acute phase of CHIKV infection determine the rate of disease progression and resolution. Annexin A1 (<i>AnxA1</i>) is involved in both initiating inflammation and preventing over-response, being essential for a balanced end of inflammation. In this study, we investigated the role of the <i>AnxA1-FPR2/ALX</i> pathway during CHIKV infection. Genetic deletion of <i>AnxA1</i> or its receptor enhanced inflammatory responses driven by CHIKV. These knockout mice showed increased neutrophil accumulation and augmented tissue damage at the site of infection compared with control mice. ConveCellsAnnexin A1-FPR2/ALX Signaling Axis Regulates Acute Inflammation during Chikungunya Virus Infection.PMC9454528MR/No17544/1Fapemig Hospedeiro em Dengue ProjectPara Mulheres na Ciência prizeInstituto Nacional de Ciência e Tecnologia em DengueSouza DGCosta VVde Araujo SMoreira TPGoncalves MRBonilha CSNogueira MLde Sousa CDFFelix FBSugimoto MACampolina-Silva GHTeixeira MMPerretti Mde Melo Costa VRSantos FMQueiroz-Junior CMfalseAnnexin A1-FPR2/ALX Signaling Axis Regulates Acute Inflammation during Chikungunya Virus Infection.Chikungunya (CHIKV) is an arthritogenic alphavirus that causes a self-limiting disease usually accompanied by joint pain and/or polyarthralgia with disabling characteristics. Immune responses developed during the acute phase of CHIKV infection determine the rate of disease progression and resolution. Annexin A1 (<i>AnxA1</i>) is involved in both initiating inflammation and preventing over-response, being essential for a balanced end of inflammation. In this study, we investigated the role of the <i>AnxA1-FPR2/ALX</i> pathway during CHIKV infection. Genetic deletion of <i>AnxA1</i> or its receptor enhanced inflammatory responses driven by CHIKV. These knockout mice showed increased neutrophil accumulation and augmented tissue damage at the site of infection compared with control mice. Conve2022-01-01T00:00:00Z2022 Aug2025-04-18T15:35:24.025Z2025-04-07T02:21:02.534ZS-EPMC94545283607812510.3390/cells11172717