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, Philip M., Foster, Paul S. and Beagley, Kenneth W. (2008) Chlamydia muridarum infection subverts dendritic cell function to promote Th2 immunity and airways hyperreactivity. Journal of Immunology, 180 4: 2225-2232.

Author Kaiko, Gerard E.
Phipps, Simon
Hickey, Danica K.
Lam, Chuan En
Hansbro, Philip M.
Foster, Paul S.
Beagley, Kenneth W.
Title Chlamydia muridarum infection subverts dendritic cell function to promote Th2 immunity and airways hyperreactivity
Journal name Journal of Immunology   Check publisher's open access policy
ISSN 0022-1767
1550-6606
Publication date 2008-02-01
Year available 2008
Sub-type Article (original research)
Open Access Status Not Open Access
Volume 180
Issue 4
Start page 2225
End page 2232
Total pages 8
Place of publication Bethesda, MD, United States
Publisher American Association of Immunologists
Language eng
Formatted abstract
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 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.
Keyword Immunology
Immunology
IMMUNOLOGY
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Biomedical Sciences Publications
 
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Created: Thu, 10 Mar 2011, 00:29:49 EST