Human Chemokine (C-C motif) Ligand 2, CCL2 ELISA Kit

This study was designed to examine the effect of yeast cell wall (YCW) supplementation on peripheral leukocyte populations and mRNA expression of cytokines in lactating dairy cows. Fourteen Holstein lactating cows were assigned to 1 of 2 treatments; the control group (n = 7) were fed a total mixed ration without supplementation and cows in the YCW group (n = 7) were fed a total mixed ration supplemented with YCW (SafMannan; Phileo, Lesaffre Animal Care, Lille, France; 10 g/cow per day). Blood samples were collected 3 times during the experimental period [wk 0 (before any treatment), wk 4, and wk 8]. Peripheral leukocyte populations and cytokine mRNA expression of peripheral blood monocular cells were measured using flow cytometry and real-time PCR, respectively. Among the peripheral leukocyte populations, TcR1-N12(+) and CD14(+) T cells increased at wk 4, and CD4(+) T cells and CD8(+) T cells increased at wk 4 and wk 8 with YCW supplementation. The mRNA level of IL8 tended to be increased in the YCW group at wk 4. Expression of IL12A was lower in the YCW group than in the control group before the experiment (wk 0) but no differences were observed at later time points (wk 4 and wk 8). Expression of IL12A decreased in the control group and increased in the YCW group. Expression of CCR2 increased at wk 4, and CCL2 and CCL3 were increased at wk 8 in the YCW group. Thus, YCW supplementation increased the mRNA expression of cytokines in peripheral blood mononuclear cells of lactating dairy cows.

Lesion healing without treatment is a unique clinical characteristic of the early stages of syphilis infection. Angiogenesis, which involves endothelial cell migration, is an important process in wound healing. Tp0136, an outer membrane protein of T. pallidum, has the ability to bind host fibronectin-producing cells, which plays a crucial role in the pathogenesis of syphilis. In this research, we purposed to analyze the role of Tp0136 in the migration of human microvascular endothelial (HMEC-1) cells and to explore the related mechanism. First, Tp0136 significantly promoted HMEC-1 cell migration. Furthermore, the levels of C-C motif ligand 2 (CCL2) mRNA and protein expression rose with the concentration and time increasing of Tp0136. The migration of HMEC-1 cells was significantly suppressed by an anti-CCL2 antibody and a CCR2 (the CCL2 receptor) inhibitor. Further study revealed that, in cells pretreated with anti-fibronectin antibody, anti-integrin beta 1 antibody or RGD (Arg-Gly-Asp), the expression levels of CCL2 induced by Tp0136 were notably decreased. Additionally, after pretreatment with an anti-fibronectin antibody, an anti-integrin beta 1 antibody or RGD, the migration of HMEC-1 cells treated with Tp0136 was obviously suppressed. These results show that Tp0136 pmmots the migration of HMEC-1 cells by inducing CCL2 expression via the interaction of the fibronectin RGD domain with integrin beta 1 and the CCL2/CCR2 signaling pathway, and these interactions may contribute to the mechanisms that increase the capacity for self-healing syphilis infection.