Chenggen Xiao1, Ping Xiao1, Xiaogang Li1, Guoqing Huang1, Hui Li2, Yusa Chen1. 1. Department of Emergency Medicine, Xiangya Hospital, Central South University Changsha 410008, Hunan, China. 2. Department of Respiratory Medicine, The First Hospital of Changsha Changsha 410005, Hunan, China.
Abstract
BACKGROUND: Infection can induce and aggravate chronic kidney disease (CKD), and the chemotaxis of Th22 cells may aggravate CKD. However, the mechanism underlying group A Streptococcus (GAS) infections in CKD through the chemotaxis of Th22 cells remains unknown. METHODS: The experiment was divided into a normal control group, an IgAN model group, a GAS-treated normal group, a GAS-treated IgAN group and an anti-CCL intervention group. An IgA nephropathy model was established, and after the success of the IgA nephropathy model was confirmed, Streptococcus haemolyticus A was inoculated intranasally and compared with treatment with anti-CCL to detect changes in Th22 cells, related chemotaxis factors and kidney pathology before and after intervention. RESULTS: An immunoglobulin A nephropathy model was successfully established. Streptococcus was successfully inoculated into the nasal cavity of the normal group and the IgA nephropathy infection control group. After intervention, pulmonary inflammatory cell infiltration was more obvious in the IgA nephropathy group than in the normal control group after Streptococcus infection. Th22 cells were detected more frequently in IgA nephropathy; after streptococcal infection, the percentage of Th22 cells in the IgAN group was higher than that in the normal group but decreased significantly when chemotaxis was blocked, the expression of CCL27, CCR10 and IL-22 declined simultaneously, and improvements in pathological changes were observed. CONCLUSION: Streptococcus may cause the chemotaxis of Th22 cells to kidney tissue, leading to or aggravating nephritis injury. AJTR
BACKGROUND: Infection can induce and aggravate chronic kidney disease (CKD), and the chemotaxis of Th22 cells may aggravate CKD. However, the mechanism underlying group A Streptococcus (GAS) infections in CKD through the chemotaxis of Th22 cells remains unknown. METHODS: The experiment was divided into a normal control group, an IgAN model group, a GAS-treated normal group, a GAS-treated IgAN group and an anti-CCL intervention group. An IgA nephropathy model was established, and after the success of the IgA nephropathy model was confirmed, Streptococcus haemolyticus A was inoculated intranasally and compared with treatment with anti-CCL to detect changes in Th22 cells, related chemotaxis factors and kidney pathology before and after intervention. RESULTS: An immunoglobulin A nephropathy model was successfully established. Streptococcus was successfully inoculated into the nasal cavity of the normal group and the IgA nephropathy infection control group. After intervention, pulmonary inflammatory cell infiltration was more obvious in the IgA nephropathy group than in the normal control group after Streptococcus infection. Th22 cells were detected more frequently in IgA nephropathy; after streptococcal infection, the percentage of Th22 cells in the IgAN group was higher than that in the normal group but decreased significantly when chemotaxis was blocked, the expression of CCL27, CCR10 and IL-22 declined simultaneously, and improvements in pathological changes were observed. CONCLUSION: Streptococcus may cause the chemotaxis of Th22 cells to kidney tissue, leading to or aggravating nephritis injury. AJTR