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Phosphocholine-Modified Lipooligosaccharides of Haemophilus influenzae Inhibit ATP-Induced IL-1beta Release by Pulmonary Epithelial Cells

dc.contributor.authorRichter, Katrin
dc.contributor.authorKoch, Christian
dc.contributor.authorPerniss, Alexander
dc.contributor.authorWolf, Philipp M.
dc.contributor.authorSchweda, Elke K. H.
dc.contributor.authorWichmann, Sven
dc.contributor.authorWilker, Sigrid
dc.contributor.authorMagel, Ilona
dc.contributor.authorSander, Michael
dc.contributor.authorMcIntosh, J. Michael
dc.contributor.authorPadberg, Winfried
dc.contributor.authorGrau, Veronika
dc.date.accessioned2022-11-18T09:54:10Z
dc.date.available2019-05-22T08:32:46Z
dc.date.available2022-11-18T09:54:10Z
dc.date.issued2018
dc.identifier.urihttp://nbn-resolving.de/urn:nbn:de:hebis:26-opus-146570
dc.identifier.urihttps://jlupub.ub.uni-giessen.de//handle/jlupub/9490
dc.identifier.urihttp://dx.doi.org/10.22029/jlupub-8878
dc.description.abstractPhosphocholine-modified bacterial cell wall components are virulence factors enabling immune evasion and permanent colonization of the mammalian host, by mechanisms that are poorly understood. Recently, we demonstrated that free phosphocholine (PC) and PC-modified lipooligosaccharides (PC-LOS) from Haemophilus influenzae, an opportunistic pathogen of the upper and lower airways, function as unconventional nicotinic agonists and efficiently inhibit the ATP-induced release of monocytic IL-1beta. We hypothesize that H. influenzae PC-LOS exert similar effects on pulmonary epithelial cells and on the complex lung tissue. The human lung carcinoma-derived epithelial cell lines A549 and Calu-3 were primed with lipopolysaccharide from Escherichia coli followed by stimulation with ATP in the presence or absence of PC or PC-LOS or LOS devoid of PC. The involvement of nicotinic acetylcholine receptors was tested using specific antagonists. We demonstrate that PC and PC-LOS efficiently inhibit ATP-mediated IL-1beta release by A549 and Calu-3 cells via nicotinic acetylcholine receptors containing subunits alpha7, alpha9, and/or alpha10. Primed precision-cut lung slices behaved similarly. We conclude that H. influenzae hijacked an endogenous anti-inflammatory cholinergic control mechanism of the lung to evade innate immune responses of the host. These findings may pave the way towards a host-centered antibiotic treatment of chronic airway infections with H. influenzae.en
dc.language.isoende_DE
dc.rightsNamensnennung 4.0 International*
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/*
dc.subjectA549en
dc.subjectCalu-3en
dc.subjectCHRNA7en
dc.subjectCHRNA9en
dc.subjectCHRNA10en
dc.subject.ddcddc:610de_DE
dc.titlePhosphocholine-Modified Lipooligosaccharides of Haemophilus influenzae Inhibit ATP-Induced IL-1beta Release by Pulmonary Epithelial Cellsen
dc.typearticlede_DE
local.affiliationFB 11 - Medizinde_DE
local.opus.id14657
local.opus.instituteLaboratory of Experimental Surgery, Department of General and Thoracic Surgeryde_DE
local.opus.fachgebietMedizinde_DE
local.source.urihttps://doi.org/10.3390/molecules23081979
local.source.freetextMolecules 23(8):1979de_DE


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