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Updated: Jun 27, 2026
06:32
Protective Efficacy and Pulmonary Immune Response Following Subcutaneous and Intranasal BCG Administration in Mice
Published on: September 19, 2016
Intranasal bacteria induce Th1 but not Treg or Th2.
M Costalonga1, P P Cleary, L A Fischer
1Department of Developmental and Surgical Sciences, School of Dentistry, University of Minnesota, Minneapolis, Minnesota, USA. costa002@umn.edu
Mucosal Immunology
|December 17, 2008
Summary
Commensal bacteria crossing the nasal barrier trigger a proinflammatory response similar to pathogens. However, these commensals, like Lactobacillus murinus, do not cause disease despite immune cell activation.
Area of Science:
- Immunology
- Microbiology
- Nasal Mucosa Immunology
Background:
- Commensal microbes colonize the nasal mucosa without causing inflammation.
- Pathogens disrupt this flora, invade tissues, and evade immune defenses.
- The adaptive immune responses differentiating commensal persistence from pathogen survival are unclear.
Purpose of the Study:
- To investigate the adaptive immune responses to commensal and pathogenic bacteria at the nasal mucosa.
- To compare the T cell activation and cytokine profiles induced by Lactobacillus murinus and Streptococcus pyogenes.
Main Methods:
- Intranasal priming of mice with L. murinus and S. pyogenes.
- Analysis of T cell responses in nasal-associated lymphoid tissue (NALT) and spleen.
- Antigen processing and presentation by NALT antigen-presenting cells were examined.
Main Results:
- The commensal L. murinus stimulated epitope-specific CD4(+) T cells less efficiently than the pathogen S. pyogenes in NALT.
- Antigen presentation in NALT involved cells other than CCR6(+) CD11c(+) dendritic cells.
- Effector/memory CD4(+) T cells induced by both microbes expressed similar proinflammatory cytokines and lacked T-regulatory markers in the spleen.
Conclusions:
- Commensals crossing the nasal epithelial barrier can elicit a proinflammatory CD4(+) T cell response akin to pathogens.
- This response occurs without inducing disease, suggesting a unique immune tolerance mechanism.
- The findings highlight distinct adaptive immune strategies for commensal persistence versus pathogen invasion.
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