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Chlamydia muridarum infection Subverts Dendritic Cell Function to promote Th2 Immunity and Airways Hyperreactivity

Kaiko, Gerard E; Phipps, Simon; Hickey, Danica K; Lam, Chuan En; Hansbro, Phil M; Foster, Paul S; Beagley, Kenneth W

Description

There is strong epidemiological evidence that Chlamydia infection can lead to exacerbation of asthma. However, the mechanism(s) whereby chlamydial infection, which normally elicits a strong Th type 1 (Th1) immune response, can exacerbate asthma, a disease characterized by dominant Th type 2 (Th2) immune responses, remains unclear. In the present study, we show that Chlamydia muridarum infection of murine bone marrow-derived dendritic cells (BMDC) modulates the phenotype, cytokine secretion...[Show more]

dc.contributor.authorKaiko, Gerard E
dc.contributor.authorPhipps, Simon
dc.contributor.authorHickey, Danica K
dc.contributor.authorLam, Chuan En
dc.contributor.authorHansbro, Phil M
dc.contributor.authorFoster, Paul S
dc.contributor.authorBeagley, Kenneth W
dc.date.accessioned2015-12-08T22:38:53Z
dc.identifier.issn0022-1767
dc.identifier.urihttp://hdl.handle.net/1885/36005
dc.description.abstractThere is strong epidemiological evidence that Chlamydia infection can lead to exacerbation of asthma. However, the mechanism(s) whereby chlamydial infection, which normally elicits a strong Th type 1 (Th1) immune response, can exacerbate asthma, a disease characterized by dominant Th type 2 (Th2) immune responses, remains unclear. In the present study, we show that Chlamydia muridarum infection of murine bone marrow-derived dendritic cells (BMDC) modulates the phenotype, cytokine secretion profile, and Ag-presenting capability of these BMDC. Chlamydia-infected BMDC express lower levels of CD80 and increased CD86 compared with noninfected BMDC. When infected with Chlamydia, BMDC secrete increased TNF-α, IL-6, IL-10, IL-12, and IL-13. OVA peptide-pulsed infected BMDC induced significant proliferation of transgenic CD4+ DO11.10 (D10) T cells, strongly inhibited IFN-γ secretion by D10 cells, and promoted a Th2 phenotype. Intratracheal transfer of infected, but not control noninfected, OVA peptide-pulsed BMDC to naive BALB/c mice, which had been i.v. infused with naive D10 T cells, resulted in increased levels of IL-10 and IL-13 in bronchoalveolar lavage fluid. Recipients of these infected BMDC showed significant increases in airways resistance and decreased airways compliance compared with mice that had received noninfected BMDC, indicative of the development of airways hyperreactivity. Collectively, these data suggest that Chlamydia infection of DCs allows the pathogen to deviate the induced immune response from a protective Th1 to a nonprotective Th2 response that could permit ongoing chronic infection. In the setting of allergic airways inflammation, this infection may then contribute to exacerbation of the asthmatic phenotype.
dc.publisherAmerican Association of Immunologists
dc.sourceJournal of Immunology
dc.subjectKeywords: B7 antigen; CD86 antigen; cytokine; interleukin 10; interleukin 12; interleukin 13; interleukin 6; tumor necrosis factor alpha; adoptive transfer; airway resistance; animal cell; animal experiment; animal model; antigen expression; antigen presentation; a
dc.titleChlamydia muridarum infection Subverts Dendritic Cell Function to promote Th2 Immunity and Airways Hyperreactivity
dc.typeJournal article
local.description.notesImported from ARIES
local.identifier.citationvolume180
dc.date.issued2008
local.identifier.absfor060199 - Biochemistry and Cell Biology not elsewhere classified
local.identifier.ariespublicationu4020362xPUB131
local.type.statusPublished Version
local.contributor.affiliationKaiko, Gerard E, University of Newcastle
local.contributor.affiliationPhipps, Simon, University of Newcastle
local.contributor.affiliationHickey, Danica K, University of Newcastle
local.contributor.affiliationLam, Chuan En, University of Newcastle
local.contributor.affiliationHansbro, Phil M, University of Newcastle
local.contributor.affiliationFoster, Paul S, College of Medicine, Biology and Environment, ANU
local.contributor.affiliationBeagley, Kenneth W, University of Newcastle
local.description.embargo2037-12-31
local.bibliographicCitation.startpage2225
local.bibliographicCitation.lastpage2232
dc.date.updated2015-12-08T10:11:44Z
local.identifier.scopusID2-s2.0-42149111673
CollectionsANU Research Publications

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