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dc.contributor.authorPausder, Alexander
dc.contributor.authorFricke, Jennifer
dc.contributor.authorSchughart, Klaus
dc.contributor.authorSchreiber, Jens
dc.contributor.authorStrowig, Till
dc.contributor.authorBruder, Dunja
dc.contributor.authorBoehme, Julia
dc.date.accessioned2022-01-18T09:55:49Z
dc.date.available2022-01-18T09:55:49Z
dc.date.issued2021-11-26
dc.identifier.citationung. 2021 Nov 26. doi: 10.1007/s00408-021-00498-8. Epub ahead of print.en_US
dc.identifier.pmid34825965
dc.identifier.doi10.1007/s00408-021-00498-8
dc.identifier.urihttp://hdl.handle.net/10033/623146
dc.description.abstractPurpose: Transport of secretory immunoglobulin A (SIgA) through the airway epithelial cell barrier into the mucosal lumen by the polymeric immunoglobulin receptor (pIgR) is an important mechanism of respiratory mucosal host defense. Identification of immunomodulating substances that regulate secretory immunity might have therapeutic implications with regard to an improved immune exclusion. Thus, we sought to analyze secretory immunity under homeostatic and immunomodulating conditions in different compartments of the murine upper and lower respiratory tract (URT&LRT). Methods: Pigr gene expression in lung, trachea, and nasal-associated lymphoid tissue (NALT) of germ-free mice, specific pathogen-free mice, mice with an undefined microbiome, as well as LPS- and IFN-γ-treated mice was determined by quantitative real-time PCR. IgA levels in bronchoalveolar lavage (BAL), nasal lavage (NAL), and serum were determined by ELISA. LPS- and IFN-γ-treated mice were colonized with Streptococcus pneumoniae and bacterial CFUs were determined in URT and LRT. Results: Respiratory Pigr expression and IgA levels were dependent on the degree of exposure to environmental microbial stimuli. While immunostimulation with LPS and IFN-γ differentially impacts respiratory Pigr expression and IgA in URT vs. LRT, only prophylactic IFN-γ treatment reduces nasal colonization with S. pneumoniae. Conclusion: Airway-associated secretory immunity can be partly modulated by exposure to microbial ligands and proinflammatory stimuli. Prophylactic IFN-γ-treatment modestly improves antibacterial immunity in the URT, but this does not appear to be mediated by SIgA or pIgR.en_US
dc.language.isoenen_US
dc.publisherSpringeren_US
dc.rightsAttribution 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectImmune modulationen_US
dc.subjectInfectionen_US
dc.subjectPolymeric immunoglobulin receptoren_US
dc.subjectRespiratory tracten_US
dc.subjectSecretory immunityen_US
dc.titleExogenous and Endogenous Triggers Differentially Stimulate Pigr Expression and Antibacterial Secretory Immunity in the Murine Respiratory Tract.en_US
dc.typeArticleen_US
dc.identifier.eissn1432-1750
dc.contributor.departmentHZI,Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7,38124 Braunschweig, Germany.en_US
dc.identifier.journalLungen_US
refterms.dateFOA2022-01-18T09:55:50Z
dc.source.journaltitleLung
dc.source.countryUnited States


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Attribution 4.0 International
Except where otherwise noted, this item's license is described as Attribution 4.0 International