Deficiency of LIGHT signaling pathway exacerbates Chlamydia psittaci respiratory tract infection in mice

Abstract

LIGHT, a costimulatory member of the immunoglobulin superfamily (Ig SF), can greatly impact T cell activation. The role of the LIGHT signaling pathway in chlamydial infection was evaluated in mice following respiratory tract infection with Chlamydia psittaci. Compared with wild type (WT) mice, LIGHT knockout (KO) mice showed significant reduction of body weight, much lower survival rate, higher bacterial burden, prolonged infection time courses and more severe pathological changes in lung tissue. The mRNA levels of IFN-γ, TNF-α, IL-17 and IL-12 in the lung tissue of LIGHT KO mice were significantly lower than those in WT mice. While there was no obvious difference in the percentages of CD4⁺ and CD8⁺ T cells in the spleens of the two groups of mice, there was a markedly elevated percentage of CD4⁺ CD25⁺ FoxP3⁺ Treg cells in LIGHT KO mice. Together, these results demonstrate that the LIGHT signaling pathway is not only required for inflammatory cytokine production as part of the host response to chlamydial infection, but also influences the differentiation of CD4⁺ CD25⁺ FoxP3⁺ Treg cells, both of which may be essential for control of C. psittaci respiratory tract infection.

Keywords: Chlamydia psittaci; LIGHT; Respiratory tract infection; T cell activation.