{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["de Araujo S"],"funding":["Fundação de Amparo à Pesquisa do Estado de Minas Gerais","Conselho Nacional de Desenvolvimento Científico e Tecnológico","Medical Research Council","L'Oréal-UNESCO-ABC"],"pagination":["2717"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9454528"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(17)"],"pubmed_abstract":["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. Conve"],"journal":["Cells"],"pubmed_title":["Annexin A1-FPR2/ALX Signaling Axis Regulates Acute Inflammation during Chikungunya Virus Infection."],"pmcid":["PMC9454528"],"funding_grant_id":["MR/No17544/1","Fapemig Hospedeiro em Dengue Project","Para Mulheres na Ciência prize","Instituto Nacional de Ciência e Tecnologia em Dengue"],"pubmed_authors":["Souza DG","Costa VV","de Araujo S","Moreira TP","Goncalves MR","Bonilha CS","Nogueira ML","de Sousa CDF","Felix FB","Sugimoto MA","Campolina-Silva GH","Teixeira MM","Perretti M","de Melo Costa VR","Santos FM","Queiroz-Junior CM"],"additional_accession":[]},"is_claimable":false,"name":"Annexin A1-FPR2/ALX Signaling Axis Regulates Acute Inflammation during Chikungunya Virus Infection.","description":"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. Conve","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Aug","modification":"2025-04-18T15:35:24.025Z","creation":"2025-04-07T02:21:02.534Z"},"accession":"S-EPMC9454528","cross_references":{"pubmed":["36078125"],"doi":["10.3390/cells11172717"]}}