Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2013
The expression of IL-2 and IL-4 in CD4(+) T cells from mouse lymph nodes and spleen during HSV-1-induced facial palsy.
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Gu Lintao, Han Yuechen, Liu Wenwen, Mao Yanyan, Li Jianfeng, Wang Haibo
Аннотация
OBJECTIVE: Herpes simplex virus 1 (HSV-1) is regarded as an important underlying cause of Bell's palsy, but the immunologic mechanism remains unknown. Here, we employed a mouse facial paralysis model to investigate the expressions of CD4(+) T lymphocytes and interleukin (IL)-2 and -4 in the left draining cervical lymph nodes (LCLN) and spleen, as well as the inhibitory effects of glucocorticoids (GCs).
METHODS: HSV-1 was inoculated into the surface of the posterior auricle to generate the facial paralysis model. The paralyzed mice were divided into three groups; in one group without any treatment, mice were killed at different time points, and those in the other two groups were injected with methylprednisolone sodium succinate (MPSS) or with a combination of MPSS and GC receptor blocker (RU486). The expression levels of CD4(+) T lymphocytes and CD4(+)-IL-2(+) and CD4(+)-IL-4(+) cells in the LCLN and spleen were detected by fluorescence-activated cell sorting.
RESULTS: Expression levels of CD4(+), IL-2, and IL-4 first increased then decreased in LCLN and spleen and peaked 5 and 7 days, respectively, after the manifestation of facial paralysis. All the data at the peak points were significantly different compared with control (p < 0.05), and these effects were inhibited by MPSS.
CONCLUSION: Our results suggest that CD4(+), IL-2, and IL-4 participate in the HSV-1-induced facial paralysis immune response. MPSS can effectively attenuate HSV-1-mediated nervous system damage, which is associated with its inhibitory effect on expression of these inflammatory markers.
METHODS: HSV-1 was inoculated into the surface of the posterior auricle to generate the facial paralysis model. The paralyzed mice were divided into three groups; in one group without any treatment, mice were killed at different time points, and those in the other two groups were injected with methylprednisolone sodium succinate (MPSS) or with a combination of MPSS and GC receptor blocker (RU486). The expression levels of CD4(+) T lymphocytes and CD4(+)-IL-2(+) and CD4(+)-IL-4(+) cells in the LCLN and spleen were detected by fluorescence-activated cell sorting.
RESULTS: Expression levels of CD4(+), IL-2, and IL-4 first increased then decreased in LCLN and spleen and peaked 5 and 7 days, respectively, after the manifestation of facial paralysis. All the data at the peak points were significantly different compared with control (p < 0.05), and these effects were inhibited by MPSS.
CONCLUSION: Our results suggest that CD4(+), IL-2, and IL-4 participate in the HSV-1-induced facial paralysis immune response. MPSS can effectively attenuate HSV-1-mediated nervous system damage, which is associated with its inhibitory effect on expression of these inflammatory markers.