Cytokine Production profiles of CD4+ T cell subsets in stressed beta2-adrenergic receptor knockout and wildtype mice during Chlamydia muridarum genital infection

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Presentation Time: 03:15 PM - 04:30 PM
Poster Board Number: B696
Abstract ID: 5472

Presenting Author:
Tesfaye Belay , Professor at Bluefield State Univ.

Abstract:

Murine CD4+ T cell subsets have distinct cytokine and transcription secretion patterns to play different functions and regulations. We demonstrated that cold-induced stress (CIS) suppresses the immune system, leading to increased intensity of Chlamydia muridaum in mice. We have reported that beta2-adrenergic receptor (b2-AR) knockout (KO) mice resist chlamydia genital infection. However, the cytokine and signature transcription profiles of CD4+ T cell subsets still need to be well explored. This study aimed to determine the cytokine production of Th1, Th2, Th17, and Treg cell types in stressed and non-stressed mice. A decrease in the production of IFN-gamma and IL-12, whereas an increase in the secretion of IL-10, IL-13, and IL-23 in CD4+ T cells of stressed wild-type mice was obtained in stressed WT mice but was restored in T cells of beta2-AR KO mice. In vitro proliferation of CD4 T cells in the presence of b2-AR antagonists, ICI 118, 551 stimulated the production of Th1 cytokines, whereas b2-AR agonist, Fenoterol, decreased the production of Th1-type cytokines but increased GATA-3, STAT-6, IL-17, IL-10, b2-AR, decreased T-bet, and STAT-4 in CD4+ T cell productions during Chlamydia muridarum genital infection was observed.  Overall, Th1 cytokine and T bet responses are reduced in stressed mice, suggesting that the cytokine status was polarized toward a Th2 immune response that can be restored by removing b2-AR from immune cells.