Dendritic cell TLR4 induces Th1-type immune response against Cryptosporidium parvum infection.

The objective of this study was to investigate the mechanism of Toll-like receptor (TLR4)- mediated dendritic cell (DC) immune against Cryptosporidium parvum infection. C. parvum sporozoites were labeled with 5,6-carboxyfluorescein diacetate succinimidyl ester. Murine bone marrow-derived DCs were isolated, and divided into TLR4 antibody blocking (TAB; infected with 2 × 105 labeled sporozoites and 0.5 µg TLR4 blocking antibody), TLR4 antibody unblocking (TAU; infected with 2 × 105 labeled sporozoites), and blank control (BC; with 1.5 mL Roswell Park Memorial Institute 1640 medium) groups. The adhesion of Cryptosporidium sporozoites to DCs and CD11c+ levels were examined by fluorescence microscopy and flow cytometry. Male KM mice were orally injected with C. parvum. The proliferation of T lymphocytes in spleen, expression of cytokines in peripheral blood, and TLR4 distribution features in different organs were further determined by immunohistochemistry. A significantly higher expression of CD11c+ and higher C. parvum sporozoite adhesion were found in the TAU group compared with other groups. The expression of CD4+CD8- /CD8+CD4- in the spleen were obviously differences between the TAB and TAU groups. The expression of TLR4, interleukin IL-4, IL-12, IL-18 and IFN-γ improved in the TAU group compared with TAB group. Higher expression of TLR4 was detected in the lymph nodes of mice in the TAU group, with pathological changes in the small intestine. Hence, TLR4 could mediate DCs to recognize C. parvum, inducing Th1 immune reaction to control C. parvum infection.

[Dynamic changes in the platelet granule membrane glycoprotein level in patients with acute myocardial infarction].

Platelet granule membrane glycoprotein (GMP-140) level was measured by using 125I labelled monoclonal antibody (SZ-51) in 20 patients with acute myocardial infarction in the first three days and at the first three weekends. The correlation of severe arrhythmia and administration of aspirin with platelet GMP-140 in AMI were studied respectively. It is shown that platelet GMP-140 increased significantly in the first three days after AMI, then it dropped quickly, but remained at high level as compared with the controlled group till the third weekend (P < 0.01). Platelet GMP-140 level was higher in the first three days than at the first three weekends (P < 0.01). The changes of platelet GMP-140 have not been shown to be related with severe arrhythmia or administration of aspirin (P > 0.05). The results indicated that the platelets in AMI are activated continuously in the first three weeks after infarction; it might be thought as an important index of coronary artery thrombus formation.