Journal
INFECTION AND IMMUNITY
Volume 75, Issue 5, Pages 2260-2268Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.01709-06
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Funding
- NHLBI NIH HHS [HL55967, R01 HL055967] Funding Source: Medline
- NIAID NIH HHS [R01 AI034343, AI34343, AI35726, AI27243, R01 AI035726, R01 AI027243] Funding Source: Medline
- NIGMS NIH HHS [T32 GM007250, T32 GM07250] Funding Source: Medline
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During pulmonary mycobacterial infection, there is increased trafficking of dendritic cells from the lungs to the draining lymph nodes. We hypothesized that ongoing mycobacterial infection would modulate recruitment and activation of antigen-specific naive CD4(+) T cells after airway antigen challenge. BALB/c mice were infected by aerosol with Mycobacterium bovis BCG. At peak bacterial burden in the lungs (4 to 6 weeks postinfection), carboxy-fluorescein diacetate succinimidyl ester-labeled naive ovalbumin-specific DO11.10 T cells were adoptively transferred into infected and uninfected mice. Recipient mice were challenged intranasally with soluble ovalbumin (OVA), and OVA-specific T-cell responses were measured in the lungs, draining mediastinal lymph nodes (MLN), and spleens. OVA challenge resulted in increased activation and proliferation of OVA-specific T cells in the draining MLN of both infected and uninfected mice. However, only BCG-infected mice had prominent OVA-specific T-cell activation, proliferation, and Th1 differentiation in the lungs. BCG infection caused greater distribution of airway OVA to pulmonary dendritic cells and enhanced presentation of OVA peptide by lung CD11c(+) cells. Together, these data suggest that an existing pulmonary mycobacterial infection alters the phenotype of lung dendritic cells so that they can activate antigen-specific naive CD4(+) T cells in the lungs in response to airway antigen challenge.
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