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To observe the dynamic changes on the bias of.Th1/Th2 responses,the mouse lung injury model was established by injection with lipopolysaccharides(LPS)via tail vein into mice and the levels of CD26~+ and CD30~+ cells were assayed by flow cytometry in order to determine the differentiation of Th1 and Th2 cells as well as the bias of Th1/Th2 responses.It was demonstrated that there was marked in- crease in the number of CD26~+ T cells in the group of mice injected with LPS 7 h after injection in com- parison with that of the control mice.The highest and lowest levels of differentiation of the CD26~+ T cells occurred at 14 h and 38 h after injection with LPS respectively,and then remained at a lower level.Simi- larly,the CD30~+ T cell differentiation was also increased at 7 h after injection and its peak was observed at 38 h after injection.In addition,all the mice injected with LPS showed definite damage of lung tissues 38 h after injection as revealed from the pathological section examinations.It is concluded from above ob- servations that the bias from the Th1 to Th2 responses and the subsequent suppression of the cell-mediated immunity may be the important cause of the LPS-induced lung injury.
To observe the dynamic changes on the bias of Th1 / Th2 responses, the mouse lung injury model was established by injection with lipopolysaccharides (LPS) via tail vein into mice and the levels of CD26 ~ + and CD30 ~ + cells were assayed by flow cytometry in order to determine the differentiation of Th1 and Th2 cells as well as the bias of Th1 / Th2 responses. It was demonstrated that there was marked in crease in the number of CD26 ~ + T cells in the group of mice injected with LPS 7 h after injection in com- parison with that of the control mice. Highest highest and lowest levels of differentiation of the CD26 ~ + T cells occurred at 14 h and 38 h after injection with LPS respectively, and then at at lower level. Simi- larly, the CD30 + T cell differentiation was also increased at 7 h after injection and its peak was observed at 38 h after injection. In addition, all the mice injected with LPS showed definite damage of lung tissues 38 h after injection as revealed from the pathological section examin ations. It is concluded from above that the bias from the Th1 to Th2 responses and the subsequent suppression of the cell-mediated immunity may be the important cause of the LPS-induced lung injury.