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dc.contributor.authorSmith-Norowitz, T A
dc.contributor.authorWeaver, D
dc.contributor.authorChorny, V
dc.contributor.authorNorowitz, Y M
dc.contributor.authorLent, D
dc.contributor.authorHammerschlag, M R
dc.contributor.authorJoks, R
dc.contributor.authorKohlhoff, S
dc.date.accessioned2023-07-07T16:47:11Z
dc.date.available2023-07-07T16:47:11Z
dc.date.issued2017-07
dc.identifier.citationSmith-Norowitz TA, Weaver D, Chorny V, Norowitz YM, Lent D, Hammerschlag MR, Joks R, Kohlhoff S. Chlamydia pneumoniae Induces Interferon Gamma Responses in Peripheral Blood Mononuclear Cells in Children with Allergic Asthma. Scand J Immunol. 2017 Jul;86(1):59-64. doi: 10.1111/sji.12561. PMID: 28480606.en_US
dc.identifier.eissn1365-3083
dc.identifier.doi10.1111/sji.12561
dc.identifier.pmid28480606
dc.identifier.urihttp://hdl.handle.net/20.500.12648/10403
dc.description.abstractRespiratory infections caused by Chlamydia pneumoniae have been associated with exacerbations of asthma. Cell-mediated immunity (CMI) is critical for maintaining immunity. We compared interferon (IFN)-γ responses in C. pneumoniae-infected peripheral blood mononuclear cells (PBMC) in paediatric patients ± asthma. Presence of C. pneumoniae was tested from asthma patients (N = 17) and non-asthmatic controls (N = 16) (PCR). PBMC were infected for 1 h ± C. pneumoniae AR-39 (MOI = 0.1) and cultured for 48 h. IFN-γ levels were measured in supernatants (ELISA). C. pneumoniae-IgG antibodies in serum were determined (MIF). All subjects tested negative for C. pneumoniae (PCR). C. pneumoniae-induced IFN-γ production in vitro was more prevalent in asthma compared with non-asthma; levels of IFN-γ were higher in asthma compared with non-asthma (P = 0.003). There was no association between recent respiratory infection and positive IFN-γ responses. These data show that C. pneumoniae modulates IFN-γ responses in patients with asthma, even in absence of active infection.
dc.language.isoenen_US
dc.relation.urlhttps://onlinelibrary.wiley.com/doi/10.1111/sji.12561en_US
dc.rights© 2017 The Foundation for the Scandinavian Journal of Immunology.
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.titleChlamydia pneumoniae Induces Interferon Gamma Responses in Peripheral Blood Mononuclear Cells in Children with Allergic Asthma.en_US
dc.typeArticle/Reviewen_US
dc.source.journaltitleScandinavian journal of immunologyen_US
dc.source.volume86
dc.source.issue1
dc.source.beginpage59
dc.source.endpage64
dc.source.countryEngland
dc.description.versionVoRen_US
refterms.dateFOA2023-07-07T16:47:12Z
html.description.abstractRespiratory infections caused by Chlamydia pneumoniae have been associated with exacerbations of asthma. Cell-mediated immunity (CMI) is critical for maintaining immunity. We compared interferon (IFN)-γ responses in C. pneumoniae-infected peripheral blood mononuclear cells (PBMC) in paediatric patients ± asthma. Presence of C. pneumoniae was tested from asthma patients (N = 17) and non-asthmatic controls (N = 16) (PCR). PBMC were infected for 1 h ± C. pneumoniae AR-39 (MOI = 0.1) and cultured for 48 h. IFN-γ levels were measured in supernatants (ELISA). C. pneumoniae-IgG antibodies in serum were determined (MIF). All subjects tested negative for C. pneumoniae (PCR). C. pneumoniae-induced IFN-γ production in vitro was more prevalent in asthma compared with non-asthma; levels of IFN-γ were higher in asthma compared with non-asthma (P = 0.003). There was no association between recent respiratory infection and positive IFN-γ responses. These data show that C. pneumoniae modulates IFN-γ responses in patients with asthma, even in absence of active infection.
dc.description.institutionSUNY Downstateen_US
dc.description.departmentPediatricsen_US
dc.description.degreelevelN/Aen_US
dc.identifier.journalScandinavian journal of immunology
dc.identifier.issue1en_US


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© 2017 The Foundation for the Scandinavian Journal of Immunology.
Except where otherwise noted, this item's license is described as © 2017 The Foundation for the Scandinavian Journal of Immunology.