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Exogenous Semaphorin 3E treatment protects against chlamydial lung infection in mice
Rony Thomas1, Shuhe Wang1, Rasheduzzaman Rashu1
1Department of Immunology, University of Manitoba, Winnipeg, MB, Canada.
Abstract:
Recent studies reported that semaphorins play a significant role in various settings of the immune response. In particular, Semaphorin 3E (Sema3E), a secreted semaphorin protein, is involved in cell proliferation, migration, inflammatory responses, and host defence against infections. However, the therapeutic function of Sema3E in bacterial infection has not been investigated. Our data showed that exogenous Sema3E treatment protects mice from chlamydial infection with lower bacterial burden, reduced body weight loss, and pathological lung changes. Cytokine analysis in the lung and spleen revealed that Sema3E-Fc treated mice, compared to saline-Fc treated mice, showed enhanced production of IFN-γ and IL-17 but reduced IL-4 and IL-10 production. Cellular analysis showed that Sema3E treatment leads to enhanced Th1/Th17 response but reduced Treg response in lungs following chlamydial infection. Moreover, Sema3E treatment also enhanced the recruitment of pulmonary dendritic cells, which express higher co-stimulatory but lower inhibitory surface molecules. The data demonstrate that Sema3E plays a vital role in protective immunity against chlamydial lung infection, mainly through coordinating functions of T cells and DCs.
Insights
Semaphorin 3E (Sema3E) protein enhances immune protection against chlamydial lung infections in mice. Sema3E treatment reduces bacterial burden and lung pathology by modulating T cell and dendritic cell responses.
Area of Science:
- Immunology
- Infectious Diseases
- Cell Biology
Background:
- Semaphorins, particularly Semaphorin 3E (Sema3E), are implicated in immune responses.
- Sema3E's role in host defense against bacterial infections remains unexplored.
- Chlamydial infections pose a significant threat to host health.
Purpose of the Study:
- To investigate the therapeutic potential of Semaphorin 3E (Sema3E) in combating chlamydial lung infections.
- To elucidate the immunological mechanisms underlying Sema3E's protective effects.
Main Methods:
- Exogenous Sema3E-Fc protein administration in a mouse model of chlamydial infection.
- Assessment of bacterial burden, body weight loss, and lung pathology.
- Analysis of cytokine profiles (IFN-γ, IL-17, IL-4, IL-10) in lung and spleen.
- Flow cytometry to evaluate T cell subsets (Th1, Th17, Treg) and dendritic cell (DC) surface molecule expression.
Main Results:
- Sema3E treatment significantly reduced bacterial load, body weight loss, and lung inflammation.
- Enhanced production of IFN-γ and IL-17, with decreased IL-4 and IL-10 levels observed in Sema3E-treated mice.
- Sema3E promoted Th1/Th17 responses while suppressing Treg responses in the lungs.
- Increased recruitment and maturation of pulmonary dendritic cells (DCs) expressing enhanced co-stimulatory molecules.
Conclusions:
- Semaphorin 3E (Sema3E) confers protective immunity against chlamydial lung infection.
- Sema3E orchestrates adaptive immune responses by modulating T cell differentiation and dendritic cell function.
- Sema3E represents a potential therapeutic target for bacterial lung infections.
