Objective To evaluate the effects of PM2.5 on the differentiation of splenic CD4 + T lymphocytes in acute asthma mice.Methods (1) Mouse models of acute asthma were established by ovalbumin (OVA) sensitization and challenge.(2) PM2.5 was collected in the urban area of Zhanjiang city under heavy traffic and serious air pollution from total suspended particulate(TSP) mid-flow sampler and multistage particles cutters and the dry powder of PM2.5 was prepared.(3) Specific-pathogen free Balb/c mice,female,at 6 to 8 weeks of age were randomly divided into 8 groups (8 mice each group):a negative control group (NC group),asthma control group (AC group),sensitized mice treated with different doses of PM2.5 groups (SP groups) and asthmatic mice treated with different doses of PM2.5 groups (AP groups).SP groups and AP groups were respectively divided into 3 subgroups according to the dose of PM2.5.The AC group,SP groups and AP groups were sensitized on D0,D7 and D14,and the NC group was treated with NS as controls.The SP1/AP1 group,SP2/AP2 group and SP3/AP3 group were respectively given 50 μL PM2.5 suspension.NC group and AC group were instilled with NS as controls.AC group and AP groups were challenged by aerosol of OVA,and NC group and SP group were treated with NS as controls.Twenty-four hours after last challenge,all the mice were sacrificed,and the percentage of regulatory T cells (Treg),T helper cell type 1 (Th1),Th2 and Th17 of splenic CD4 + T lymphocytes was detected by flow cytometry (FCM).Results (1) An OVA-induced mouse models with acute asthma were successfully established.(2) Comparison of the percentage of Treg of splenic CD4 + T lymphocytes:SP group [(12.28 ± 0.73) ％,(11.93 ± 0.81) ％ and (11.70-± 1.14) ％] and AC group [(12.18 ± 1.00) ％] were lower than that in the NC group[(13.50 ± 0.39) ％] (P ＜ 0.05),AP3 group [(10.58 ± 0.65) ％] was lower than that in the AC group and AP1 group [(11.91 ± 0.79) ％] (P ＜ 0.05).(3) Comparison of the ratio of Th1/Th2 of splenic CD4+ T lymphocyte:SP1 group [(7.74 ± 1.21)％] was higher than that in the NC group [(5.52 ± 1.06) ％] (P ＜0.05),SP2 group[(6.30 ±0.58) ％] was lower than that in the SP1 group(P ＜0.05),SP3 group [(4.87 ± 0.82) ％] was lower than that in the SP2 group (P ＜ 0.05);AC group [(3.69-± 0.47) ％] was lower than that in the NC group and SP3 group (P ＜ 0.05);AP3 group [(2.92 ± 0.57) ％] was lower than that in the AC group(P ＜ 0.05).(4) Comparison of the percentage of Th17 of splenic CD4+ T lymphocyte:AP3 group [(1.46 ± 0.39) ％] was higher than that in the NC group [(0.89 ± 0.24) ％] and the AP2 group [(0.83 ± 0.15) ％] (P ＜ 0.001).Conclusions PM2.5 can inhibit splenic CD4 + T lymphocyte of acute asthma mice differentiation into Treg and Th1,and promote their differentiation into Th2 and Th17,through which aggravates inflammation reactions in the airway.

Objective The present study aimed to explore the effects of CC-chemokine receptor 5 antagonism on tumor growth and immune microenvironment.Methods Cell Counting Kit-8 was used to detect in vitro anti-proliferation activity of maraviroc,a selective CC-chemokine receptor 5 inhibitor,on Lewis cells,a mouse lung adenocarcinoma cell strain.Flow cytometry and real-time quantitative PCR were respectively used to detect cell apop-tosis and Caspase 8 gene expression.In a congenic mouse lung cancer model,the mice were intraperitoneally admin-istered with maraviroc or vehicle.Tumor sizes were measured and tumor infiltrating CD4+,CD8+ and Foxp3+ cells were determined by immunofluorescent staining.Results Our results showed that maraviroc could inhibit the growth of Lewis cancer cells not only in vitro but also in vivo.This in-vitro inhibition was presumably attributable to apoptosis induction by the enhancement of Caspase 8 gene expression after maraviroc blockade.Additionally,more CD4+ and CD8+ cells but less Foxp3+ cells were detected in tumor mass from the mice administered with maraviroc.Conclusions Taken together,it can be speculated that CCR5 blockade may inhibit the growth of Lewis cells by inducing cell apoptosis and impairing the immunosuppressive tumor microenvironment.It is worthy of further investi-gation as a candidate for cancer therapy.

Diabetic nephropathy is one of the most common microvascular complications of diabetes. It is the main cause of end-stage renal disease and a cause of increased mortality of diabetes. Moreover， diabetic nephropathy has a complex pathogenesis， which is difficult to be detected in the early stage. Therefore， it is easy to miss the optimal intervention period in clinical treatment， which seriously endangers the life and health of patients. As an active ingredient of Chinese medicine， polysaccharides have biological activities such as anti-tumor， lowering blood sugar， immune regulation， anti-oxidation and anti-virus. In recent years， many studies have demonstrated that polysaccharides in Chinese medicine can effectively interfere with diabetic nephropathy， with multi-target and multi-channel characteristics and significant effect， showing great potential. Although there are many studies on the mechanism of Chinese medicine polysaccharides in the intervention of diabetic nephropathy， there is a lack of a systematic and detailed review on it. Therefore， based on the animal experiments on the intervention of Chinese medicine polysaccharides in diabetic nephropathy in recent years， we analyzed and summarized the mechanism of Chinese medicine polysaccharides in the intervention of diabetic nephropathy from five aspects of improving insulin resistance， improving oxidative stress， reducing inflammatory reaction， protecting kidney and improving intestinal flora. In addition， the signaling pathways and indicators involved in the mechanism were summarized， and the intervention effect and polysaccharide structure analysis were compared. The paper was expected to provide a theoretical basis for the basic research， new drug development and clinical application of Chinese medicine polysaccharides in the intervention of diabetic nephropathy.