CD103+ Cells and Chemokine Receptor Expression in Breast Cancer.

Mucosal environments harbour lymphocytes, which express several adhesion molecules, including intestinal homing receptors and integrin αE/ß7 (CD103). CD103 binds E-cadherin, an integrin receptor expressed in intestinal endothelial cells. Its expression not only enables homing or retention of T lymphocytes at these sites but is also associated with increased T lymphocyte activation. However, it is not yet clear how CD103 expression is related to the clinical staging of breast cancer, which is determined by factors such as the size of the tumor (T), the involvement of nearby lymph nodes (N), and presence of metastasis (M). We examined the prognostic significance of CD103 by FACS in 53 breast cancer patients and 46 healthy controls enrolled, and investigated its expression, which contributes to lymphocyte recruitment in tumor tissue. Patients with breast cancer showed increased frequencies of CD103+, CD4+CD103+, and CD8+CD103+ cells compared to controls. CD103 was expressed at a high level on the surfaces of tumor-infiltrating lymphocytes in patients with breast cancer. Its expression in peripheral blood was not correlated with clinical TNM stage. To determine the localisation of CD103+ cells in breast tissue, tissue sections of breast tumors were stained for CD103. In tissue sections of breast tumors stained for CD103, its expression in T lymphocytes was higher compared to normal breast tissue. In addition, CD103+ cells expressed higher levels of receptors for inflammatory chemokines, compared to CD103- cells. CD103+ cells in peripheral blood and tumor tissue might be an important source of tumor-infiltrating lymphocyte trafficking, homing, and retention in cancer patients.

Receptor for activated C kinase 1 in rats with ischemia-reperfusion injury: intravenous versus inhalation anaesthetic agents.

Background: The study examined the difference in the expression of the receptor for activated C kinase 1 (RACK1) between anaesthesia with propofol and isoflurane in rats with myocardial ischemia-reperfusion injury (IRI). Methods: Male Sprague-Dawley rats were studied. Anaesthesia was induced with xylazine 20 µg/g by intraperitoneal injection and maintained with propofol or isoflurane. Myocardial IRI was induced by ligating the left anterior descending artery for 1 hour. Reactive oxygen species (ROS), cardiomyocyte apoptosis, the expression of RACK1 and toll-like receptor 4 (TLR4), and the heart injury score were compared between the two groups. Results: Cardiomyocyte apoptosis with ROS was significantly lower in the propofol group than in the isoflurane group. The propofol group had significantly higher RACK1 expression and lower TLR4 expression, compared with the isoflurane group (RACK1, 1970.50 ± 120.50 vs. 1350.20 ± 250.30, p<0.05; TLR4, 980.50 ± 110.75 vs. 1275.50 ± 75.35, p<0.05). However, the heart injury scores in the two groups did not differ significantly (3.56 ± 0.29 vs. 4.33 ± 0.23 in the propofol and isoflurane groups, respectively, p=0.33). Conclusion: There were significant differences in inflammation and apoptosis, including the expression of RACK1 and TLR4, after myocardial IRI between the propofol and isoflurane groups. However, both groups had similar heart injury scores.

Effects of Glycyrrhizin on the Differentiation of Myeloid Cells of the Heart and Lungs in Lipopolysaccharide-Induced Septic Mice.

BACKGROUND: This study investigated the effects of glycyrrhizin (GR) on the ratio of myeloid-derived suppressor cells (MDSCs) to cluster of differentiation (CD)11b+Gr1 myeloid cells in the heart and lungs in lipopolysaccharide (LPS)-induced septic mice. METHODS: Mice were divided into three groups: Control, LPS, and LPS+GR. After intraperitoneal injection of phosphate-buffered saline for the Control group, LPS for the LPS group, and a combination of LPS and GR for the LPS+GR group, fluorescence-activated cell sorting was utilized to evaluate cytokines and immune cells in the blood, heart, and lungs. Histopathologic analysis of Toll-like receptor (TLR)4 was also performed. RESULTS: The cytokine amounts in the LPS and LPS+GR groups were significantly higher than in the Control group; however, that in the LPS+GR group was significant lower than in the LPS group. The ratio of MDSCs to CD11b+Gr1 myeloid cells in the LPS+GR group was significantly higher than in the LPS group but was significantly lower than in the Control group. The staining intensity of TLR4 showed the same pattern as that of cytokines in the heart and lungs. TLR4 staining was significantly lower in the LPS+GR group than in the LPS group but was higher than that in the Control group. CONCLUSION: GR exhibited protective effects on the heart and lungs in LPS-induced septic mice. The effects were associated with an elevated ratio of MDSCs to CD11b+Gr1 myeloid cells and the inhibition of cytokine release and TLR4 expression after GR injection.