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Azithromycin improves macrophage phagocytic function and expression of mannose receptor in chronic obstructive pulmonary disease

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dc.contributor.authorHodge, S.
dc.contributor.authorHodge, G.
dc.contributor.authorJersmann, H.
dc.contributor.authorMatthews, G.
dc.contributor.authorAhern, J.
dc.contributor.authorHolmes, M.
dc.contributor.authorReynolds, P.
dc.date.issued2008
dc.descriptionCopyright © 2008 American Thoracic Society
dc.description.abstractRationale: Defective efferocytosis (phagocytic clearance of apoptotic cells) in the airway may perpetuate inflammation via secondary necrosis in chronic obstructive pulmonary disease (COPD). We have previously reported that low-dose azithromycin improved alveolar macrophage (AM) phagocytic function in vitro. Objectives: We investigated collectins (mannose-binding lectin [MBL] and surfactant protein [SP]-D) and mannose receptor (MR) in COPD and their possible role in the azithromycin-mediated improvement in phagocytosis. Methods: In vitro effects of azithromycin on AM expression of MR were investigated. MBL, SP-D, and MR were measured in patients with COPD and control subjects. Azithromycin (250 mg orally daily for 5 d then twice weekly for 12 wk) was administered to 11 patients with COPD. Assessments included AM phagocytic ability and expression of MR, MBL, SP-D, bronchial epithelial cell apoptosis, pulmonary function, C-reactive protein, blood/BAL leukocyte counts, cytokine production, and T-cell markers of activation and phenotype. Measurements and Main Results: Azithomycin (500 ng/ml) increased MR expression by 50% in vitro. AM MR expression and levels of MBL and SP-D were significantly reduced in patients with COPD compared with control subjects. In patients with COPD, after azithromycin therapy, we observed significantly improved AM phagocytic ability (pre: 9.9%; post: 15.1%), reduced bronchial epithelial cell apoptosis (pre: 30.0%; post: 19.7%), and increased MR and reduced inflammatory markers in the peripheral blood. These findings implicate the MR in the defective phagocytic function of AMs in COPD and as a target for the azithromycin-mediated improvement in phagocytic ability. Conclusions: Our findings indicate a novel approach to supplement existing therapies in COPD.
dc.description.statementofresponsibilitySandra Hodge, Greg Hodge, Hubertus Jersmann, Geoffrey Matthews, Jessica Ahern, Mark Holmes and Paul N. Reynolds
dc.identifier.citationAmerican Journal of Respiratory and Critical Care Medicine, 2008; 178(2):139-148
dc.identifier.doi10.1164/rccm.200711-1666OC
dc.identifier.issn1073-449X
dc.identifier.issn1535-4970
dc.identifier.orcidHodge, S. [0000-0002-3602-9927] [0000-0002-9401-298X]
dc.identifier.orcidJersmann, H. [0000-0003-1763-2736]
dc.identifier.orcidReynolds, P. [0000-0002-2273-1774]
dc.identifier.urihttp://hdl.handle.net/2440/51898
dc.language.isoen
dc.publisherAmerican Thoracic Society
dc.source.urihttps://doi.org/10.1164/rccm.200711-1666oc
dc.subjectchronic obstructive pulmonary disease
dc.subjectalveolar macrophage
dc.subjectphagocytosis
dc.subjectazithromycin
dc.subjectapoptosis
dc.titleAzithromycin improves macrophage phagocytic function and expression of mannose receptor in chronic obstructive pulmonary disease
dc.typeJournal article
pubs.publication-statusPublished

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