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dc.contributor.authorGalvao-Filho, Bruno
dc.contributor.authorde Castro, Julia Teixeira
dc.contributor.authorFigueiredo, Maria Marta
dc.contributor.authorRosmaninho, Claudio Goncalves
dc.contributor.authorAntonelli, Lis Ribeiro do Valle
dc.contributor.authorGazzinelli, Ricardo T.
dc.date2022-08-11T08:09:52.000
dc.date.accessioned2022-08-23T16:47:05Z
dc.date.available2022-08-23T16:47:05Z
dc.date.issued2019-03-01
dc.date.submitted2019-05-16
dc.identifier.citation<p>Mucosal Immunol. 2019 Mar;12(2):312-322. doi: 10.1038/s41385-018-0093-5. Epub 2018 Oct 18. <a href="https://doi.org/10.1038/s41385-018-0093-5">Link to article on publisher's site</a></p>
dc.identifier.issn1933-0219 (Linking)
dc.identifier.doi10.1038/s41385-018-0093-5
dc.identifier.pmid30337650
dc.identifier.urihttp://hdl.handle.net/20.500.14038/41009
dc.description.abstractMalaria-associated acute respiratory distress syndrome (MA-ARDS) and acute lung injury (ALI) are complications that cause lung damage and often leads to death. The MA-ARDS/ALI is associated with a Type 1 inflammatory response mediated by T lymphocytes and IFN-gamma. Here, we used the Plasmodium berghei NK65 (PbN)-induced MA-ALI/ARDS model that resembles human disease and confirmed that lung CD4(+) and CD8(+) T cells predominantly expressed Tbet and IFN-gamma. Surprisingly, we found that development of MA-ALI/ARDS was dependent on functional CCR4, known to mediate the recruitment of Th2 lymphocytes and regulatory T cells. However, in this Type 1 inflammation-ARDS model, CCR4 was not involved in the recruitment of T lymphocytes, but was required for the emergence of TNF-alpha/iNOS producing dendritic cells (Tip-DCs) in the lungs. In contrast, recruitment of Tip-DCs and development of MA-ALI/ARDS were not altered in CCR2(-/)(-) mice. Importantly, we showed that NOS2(-/)(-) mice are resistant to PbN-induced lung damage, indicating that reactive nitrogen species produced by Tip-DCs play an essential role in inducing MA-ARDS/ALI. Lastly, our experiments suggest that production of IFN-gamma primarily by CD8(+) T cells is required for inducing Tip-DCs differentiation in the lungs and the development of MA-ALI/ARDS model.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=30337650&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6375779/
dc.subjectHemic and Immune Systems
dc.subjectImmunology and Infectious Disease
dc.subjectParasitic Diseases
dc.subjectPathological Conditions, Signs and Symptoms
dc.subjectRespiratory Tract Diseases
dc.titleThe emergence of pathogenic TNF/iNOS producing dendritic cells (Tip-DCs) in a malaria model of acute respiratory distress syndrome (ARDS) is dependent on CCR4
dc.typeJournal Article
dc.source.journaltitleMucosal immunology
dc.source.volume12
dc.source.issue2
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/3805
dc.identifier.contextkey14516656
html.description.abstract<p>Malaria-associated acute respiratory distress syndrome (MA-ARDS) and acute lung injury (ALI) are complications that cause lung damage and often leads to death. The MA-ARDS/ALI is associated with a Type 1 inflammatory response mediated by T lymphocytes and IFN-gamma. Here, we used the Plasmodium berghei NK65 (PbN)-induced MA-ALI/ARDS model that resembles human disease and confirmed that lung CD4(+) and CD8(+) T cells predominantly expressed Tbet and IFN-gamma. Surprisingly, we found that development of MA-ALI/ARDS was dependent on functional CCR4, known to mediate the recruitment of Th2 lymphocytes and regulatory T cells. However, in this Type 1 inflammation-ARDS model, CCR4 was not involved in the recruitment of T lymphocytes, but was required for the emergence of TNF-alpha/iNOS producing dendritic cells (Tip-DCs) in the lungs. In contrast, recruitment of Tip-DCs and development of MA-ALI/ARDS were not altered in CCR2(-/)(-) mice. Importantly, we showed that NOS2(-/)(-) mice are resistant to PbN-induced lung damage, indicating that reactive nitrogen species produced by Tip-DCs play an essential role in inducing MA-ARDS/ALI. Lastly, our experiments suggest that production of IFN-gamma primarily by CD8(+) T cells is required for inducing Tip-DCs differentiation in the lungs and the development of MA-ALI/ARDS model.</p>
dc.identifier.submissionpathoapubs/3805
dc.contributor.departmentDepartment of Medicine, Division of Infectious Diseases and Immunology
dc.source.pages312-322


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