title: Type 1 T-cell responses in chlamydial lung infections are associated with local MIP-1alpha response.
abstract: Chemokines and their receptors are important mediators of leukocyte trafficking and recruitment and sometimes work as modulators of T-cell responses during infections and inflammation. Modulating the biological activity of chemokines has been found to influence the course of diseases. However, little is known about the role of chemokine responses during chlamydial lung infections. We therefore analyzed the dynamics of multiple chemokines, which are frequently associated with type 1 (Th1) T cell immune responses, and their receptors for their expression in the lungs during Chlamydia muridarum (Cm) infections. We also examined the relationship between chemokine responses and the development of Th1 responses as well as the clearance of infection. Our results showed that in parallel with the high levels of gamma interferon (IFN-gamma) and IL-12 production in the lungs and draining lymph nodes, and the expansion of IFN-gamma-producing CD4 and CD8+ T cells, the production of the cell-related chemokines RANTES, IFN-gamma-inducible protein-10 (IP-10) and macrophage inflammatory protein-1alpha (MIP-1alpha) and their receptor CCR1 was elevated in the lung tissues after infection. Interestingly, in a later phase of infection, the expression of RANTES and IP-10 remained elevated but the expression of MIP-1alpha and CCR1 decreased to a low level, which suggests a closer association with the pattern of Th1 cytokine responses in the process of infection. These results suggest a close association between the MIP-1alpha response and the Th1-type T-cell responses in chlamydial lung infections.
authors.affiliation: Department of Immunology, Tianjin Medical University, Tianjin Key Laboratory of Cellular and Molecular Immunology, Key Laboratory of Educational Ministry of China, Tianjin, China.
authors.forename: Naihong
authors.initials: N
authors.lastname: Zhang
authors.forename: Zhaoe
authors.initials: Z
authors.lastname: Wang
authors.forename: Xiaofei
authors.initials: X
authors.lastname: Tang
authors.forename: Haiping
authors.initials: H
authors.lastname: Wang
authors.forename: Hongzhao
authors.initials: H
authors.lastname: Li
authors.forename: Huanjun
authors.initials: H
authors.lastname: Huang
authors.forename: Hong
authors.initials: H
authors.lastname: Bai
authors.forename: Xi
authors.initials: X
authors.lastname: Yang
mesh_terms: D000818:Animals; D054405:Chemokine CCL3 / Q000096:biosynthesis / Q000276:immunology*; D002690:Chlamydia Infections / Q000276:immunology* / Q000378:metabolism; D023502:Chlamydia muridarum / Q000276:immunology*; D005260:Female; D005786:Gene Expression Regulation; D006367:HeLa Cells; D006801:Humans; D007371:Interferon-gamma / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D018664:Interleukin-12 / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D018410:Pneumonia, Bacterial / Q000276:immunology* / Q000378:metabolism; D018417:Th1 Cells / Q000276:immunology*
chemical_list: D054405:Chemokine CCL3; D018664:Interleukin-12; D007371:Interferon-gamma