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Characterization of Inflammatory Responses During Intranasal Colonization with Streptococcus pneumoniae
Published on: January 17, 2014
Effects of recombinant IL-17F intranasal inoculation against Streptococcus pneumoniae infection in a murine model
Ling Chen1, Sheng Guo1, Liangxia Wu1
1Department of Pediatrics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiaotong University, Shanghai, 200233, People's Republic of China.
Abstract:
Interleukin-17F (IL-17F) is an important member of IL-17 cytokine family, which plays important roles in host defense against microbial infections. Streptococcus pneumoniae is a common pathogen associated with several invasive and noninvasive pneumococcal diseases, and mucosal immune response plays crucial roles in defenses against pneumococcal infection. Thus, intranasal inoculation may be an alternative approach against pneumococci. In this study, BALB/c mice were intranasally inoculated with recombinant IL-17F (rIL-17F) prior to S. pneumoniae (American Type Culture Collection 6303, serotype 3) infection. As compared with the control group, numbers of total leukocyte, neutrophil, and macrophage in lungs were significantly increased in mice inoculated with rIL-17F. The levels of macrophage inflammatory protein 1α (MIP-1α), MIP-2β, and interferon γ were significantly increased in bronchoalveolar lavage fluid and culture supernatant of splenocytes from mice inoculated with rIL-17F. rIL-17F inoculation also significantly elevated β-defensin-2 expression in lung tissues. Furthermore, compared with S. pneumoniae infection group, rIL-17F inoculation prior to infection significantly reduced S. pneumoniae colonization in lungs. These findings demonstrated that rIL-17F intranasal inoculation strengthened host defense against pneumococci, which may be developed to prevent pneumococcal infection.
Insights
Intranasal interleukin-17F (IL-17F) boosts lung immunity against Streptococcus pneumoniae. This approach enhances immune cell activity and reduces bacterial colonization, offering a potential strategy for preventing pneumococcal infections.
Area of Science:
- Immunology
- Microbiology
- Respiratory Medicine
Background:
- Interleukin-17F (IL-17F) is a key cytokine in host defense against microbial infections.
- Streptococcus pneumoniae causes significant pneumococcal diseases, necessitating effective mucosal immune responses.
- Intranasal administration is explored as a potential delivery route for immune stimulation against pneumococci.
Purpose of the Study:
- To investigate the efficacy of intranasal recombinant IL-17F (rIL-17F) in enhancing host defense against Streptococcus pneumoniae infection.
- To evaluate the impact of rIL-17F on immune cell infiltration and inflammatory mediator production in the lungs.
- To assess the effect of rIL-17F pre-treatment on pneumococcal colonization in mice.
Main Methods:
- BALB/c mice were intranasally inoculated with rIL-17F before infection with Streptococcus pneumoniae.
- Immune cell counts (leukocytes, neutrophils, macrophages) in the lungs were analyzed.
- Levels of inflammatory mediators (MIP-1α, MIP-2β, IFN-γ) in bronchoalveolar lavage fluid and splenocyte cultures were measured.
- Lung tissue expression of β-defensin-2 was assessed.
- Bacterial colonization in the lungs was quantified.
Main Results:
- rIL-17F inoculation significantly increased total leukocyte, neutrophil, and macrophage numbers in the lungs.
- Elevated levels of MIP-1α, MIP-2β, and interferon-γ were observed in response to rIL-17F.
- β-defensin-2 expression was significantly upregulated in lung tissues following rIL-17F administration.
- Pre-treatment with rIL-17F significantly reduced Streptococcus pneumoniae colonization in the lungs compared to infection alone.
Conclusions:
- Intranasal administration of rIL-17F effectively enhances the mucosal immune response against Streptococcus pneumoniae.
- rIL-17F strengthens host defense mechanisms, including immune cell recruitment and antimicrobial peptide production.
- This study suggests that intranasal rIL-17F is a promising strategy for the prevention of pneumococcal infections.

