In breast cancer, sentinel lymph nodes (SLNs) represent the first site of interaction between tumor-derived antigens and the host immune system. However, descriptive data on immune cell subsets within the SLN remains limited. This exploratory study evaluated immune cell populations in SLN samples from women with invasive breast cancer (IBC) using flow cytometry, and assessed their distribution according to clinicopathological characteristics.SNL scrapings were collected from 22 patients with IBC. SNL cells were evaluated using flow cytometry, and the results were compared with clinical and pathological variables, such as tumor subtype, axillary status, lymphovascular invasion (LVI), histological grades, and expression of estrogen receptors (ERs) and human epidermal growth factor receptor 2 (HER2). The frequencies of monocytes and neutrophils were not significantly correlated with the clinical variables analyzed. In patients with LVI, there was an increase in the frequency of CD4+ T cells and programmed death-1 (PD-1) expression in CD8+ T-cells.Furthermore, a reduction in central memory CD4+ T cells and an increase in terminal effector memory CD4+ T cells were observed in patients with histological grade III disease compared to those with histological grade I disease. It was also observed that in patients expressing ERs and HER2, there was an increase in PD-1 and programmed death-ligand 1 expression in CD8+ T-cells. These findings provide a descriptive overview of immune cell distribution in SLNs according to their clinicopathological features. These results are preliminary and hypothesis-generating, supporting the need for larger longitudinal studies to further characterize the immune profiles within tumor-draining lymph nodes.

Background: Activation of the mitogen-activated protein kinase (MAPK) pathway induces uncontrolled cell proliferation in response to inflammatory stimuli. Adriamycin (ADR)-induced nephropathy (ADRN) in rats triggers MAPK activation and pro-inflammatory mechanisms by increasing cytokine secretion, similar to chronic kidney disease (CKD). Activation of the vitamin D receptor (VDR) plays a crucial role in suppressing the expression of inflammatory markers in the kidney and may contribute to reducing cellular proliferation. This study evaluated the effect of pre-treatment with paricalcitol on ADRN in renal inflammation mechanisms. Methods: Male Sprague-Dawley rats were implanted with an osmotic minipump containing activated vitamin D (paricalcitol, Zemplar, 6 ng/day) or vehicle (NaCl 0.9%). Two days after implantation, ADR (Fauldoxo, 3.5 mg/kg) or vehicle (NaCl 0.9%) was injected. The rats were divided into four experimental groups: control, n = 6; paricalcitol, n = 6; ADR, n = 7 and, ADR + paricalcitol, n = 7. Results: VDR activation was demonstrated by increased CYP24A1 in renal tissue. Paricalcitol prevented macrophage infiltration in the glomeruli, cortex, and outer medulla, prevented secretion of tumor necrosis factor-α, and interleukin-1β, increased arginase I and decreased arginase II tissue expressions, effects associated with attenuation of MAPK pathways, increased zonula occludens-1, and reduced cell proliferation associated with proliferating cell nuclear antigen expression. Paricalcitol treatment decreased the stromal cell-derived factor 1α/chemokine C-X-C receptor type 4/β-catenin pathway. Conclusions Paricalcitol plays a renoprotective role by modulating renal inflammation and cell proliferation. These results highlight potential targets for treating CKD.

This study was conducted to investigate the occurrence of oxidative stress in the heart tissue of rats infected with Trypanosoma evansi. Rats were divided into 2 groups (A and B) with 12 animals each, and further subdivided into 4 subgroups (A1 and A2, 6 animals/each; and B1 and B2, 6 animals/each). Animals in the groups B1 and B2 were subcutaneously inoculated with T. evansi. Thiobarbituric acid reactive substances (TBARS), superoxide dismutase activity (SOD), glutathione S-transferase activity (GST), reduced glutathione activity (GSH), and non-protein thiols (NPSH) in the heart tissue were evaluated. At day 5 and 15 post-infection (PI), an increase in the TBARS levels and a decrease in the SOD activity (P<0.05) were observed. GSH and GST activities were decreased in infected animals at day 15 PI (P<0.05). Considering the proper functioning of the heart, it is possible that the changes in the activity of these enzymes involved in the oxidative stress may be related, at least in part, in the pathophysiology of rats infected with T. evansi.
Animals ; Glutathione ; Glutathione Transferase ; Heart* ; Oxidative Stress* ; Rats* ; Sulfhydryl Compounds ; Superoxide Dismutase ; Thiobarbituric Acid Reactive Substances ; Trypanosoma*