Chronic ethanol exposure impairs alveolar leukocyte infiltration during pneumococcal pneumonia, leading to an increased bacterial burden despite increased CXCL1 and nitric oxide levels

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dc.creatorFlávia Rayssa Braga Martins
dc.creatorMaycon Douglas de Oliveira
dc.creatorJéssica Amanda Marques Souza
dc.creatorCelso Martins Queiroz-Junior
dc.creatorFrancisco Pereira Lobo
dc.creatorMauro Martins Teixeira
dc.creatorNathalia Luisa Malacco
dc.creatorFrederico Marianetti Soriani
dc.date.accessioned2025-01-21T20:44:27Z
dc.date.accessioned2025-09-08T23:47:23Z
dc.date.available2025-01-21T20:44:27Z
dc.date.issued2023-05-19
dc.format.mimetypepdf
dc.identifier.doihttps://doi.org/10.3389/fimmu.2023.1175275
dc.identifier.issn1664-3224
dc.identifier.urihttps://hdl.handle.net/1843/79380
dc.languageeng
dc.publisherUniversidade Federal de Minas Gerais
dc.relation.ispartofFrontiers in Immunology
dc.rightsAcesso Aberto
dc.subjectÁlcool no organismo
dc.subjectInflamação
dc.subjectFatores de risco
dc.subjectMicrobiologia
dc.subjectPneumonia
dc.subjectSaúde pública
dc.subject.otherAlcohol
dc.subject.otherNitric oxide
dc.subject.otherPneumonia
dc.subject.otherStreptococcus pneumoniae
dc.subject.otherCXCL1
dc.titleChronic ethanol exposure impairs alveolar leukocyte infiltration during pneumococcal pneumonia, leading to an increased bacterial burden despite increased CXCL1 and nitric oxide levels
dc.typeArtigo de periódico
local.citation.epage9
local.citation.spage1
local.citation.volume14
local.description.resumoEthanol abuse is a risk factor for the development of pneumonia caused by Streptococcus pneumoniae, a critical pathogen for public health. The aim of this article was to investigate the inflammatory mechanisms involved in pneumococcal pneumonia that may be associated with chronic ethanol exposure. Male C57BL6/J-Unib mice were exposed to 20% (v/v) ethanol for twelve weeks and intranasally infected with 5x104 CFU of S. pneumoniae. Twenty-four hours after infection, lungs, bronchoalveolar lavage and blood samples were obtained to assess the consequences of chronic ethanol exposure during infection. Alcohol-fed mice showed increased production of nitric oxide and CXCL1 in alveoli and plasma during pneumococcal pneumonia. Beside this, ethanol-treated mice exhibited a decrease in leukocyte infiltration into the alveoli and reduced frequency of severe lung inflammation, which was associated with an increase in bacterial load. Curiously, no changes were observed in survival after infection. Taken together, these results demonstrate that chronic ethanol exposure alters the inflammatory response during S. pneumoniae lung infection in mice with a reduction in the inflammatory infiltrate even in the presence of higher levels of the chemoattractant CXCL1.
local.identifier.orcidhttps://orcid.org/0009-0006-8076-5207
local.identifier.orcidhttps://orcid.org/0009-0000-8063-0595
local.identifier.orcidhttps://orcid.org/0009-0002-3775-7333
local.identifier.orcidhttps://orcid.org/0009-0004-3318-4667
local.identifier.orcidhttps://orcid.org/0000-0002-9671-9313
local.identifier.orcidhttps://orcid.org/0000-0002-6944-3008
local.identifier.orcidhttps://orcid.org/0000-0002-7612-3651
local.identifier.orcidhttps://orcid.org/0000-0003-4720-6746
local.publisher.countryBrasil
local.publisher.departmentICB - DEPARTAMENTO DE BIOQUÍMICA E IMUNOLOGIA
local.publisher.departmentICB - DEPARTAMENTO DE FARMACOLOGIA
local.publisher.departmentICB - DEPARTAMENTO DE MORFOLOGIA
local.publisher.initialsUFMG
local.url.externahttps://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2023.1175275/full

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