Air pollutants and their interaction with environmental allergens have been considered as an important reason for the recent increase in the prevalence of allergic diseases. The aim of this study was to investigate the traffic pollution effect, as a stressor, on Platanus orientalis pollen allergens messenger RNA (mRNA) and protein expression. P. orientalis pollen grains were collected along main streets of heavy traffic and from unpolluted sites in Mashhad city, in northeast Iran. The pollen samples were examined by scanning electron microscopy. To assess the abundance of pollen allergens (Pla or 1, Pla or 2, and Pla or 3) from polluted and unpolluted sites, immunoblotting was performed. Moreover, the sequences encoding P. orientalis allergens were amplified using real-time PCR. Scanning electron microscopy showed a number of particles of 150-550 nm on the surface of pollen from polluted sites. Also, protein and gene expression levels of Pla or 1 and Pla or 3 were considerably greater in pollen samples from highly polluted areas than in pollen from unpolluted areas (p < 0.05). In contrast, no statically significant difference in Pla or 2 protein and mRNA expression level was found between samples from the two areas. We found greater expression of allergens involved in plant defense mechanisms (Pla or 1 and Pla or 3) in polluted sites than in unpolluted ones. The high expression of these proteins can lead to an increase in the prevalence of allergic diseases. These findings suggest the necessity of supporting public policies aimed at controlling traffic pollution to improve air quality and prevent the subsequent clinical outcomes and new cases of asthma.
The impact of immunization with gentamicin-attenuated Leishmania infantum (H-line) on the immunophenotypic profile of popliteal lymph node (PLN) and peripheral blood mononuclear cells (PBMCs) of dogs was assessed by flow cytometry and immunohistochemistry. Compared with the dogs infected with L. infantum wild-type (Group WT), there was a significantly higher percentage of CD4+, CD44+ T cells and CD14+, MHC-II+ cells and a lower percentage of CD4+ CD25+ regulatory T cells in PLN of the immunized dogs with L. infantum H-line (Group H). The percentage of CD4+ and CD8+ T cells in PBMCs of immunized dogs was higher than that in dogs of Group WT. The CD4:CD8 ratio in PLN of dogs of Group H was significantly higher than that in dogs of Group WT. A significantly higher percentage of CD21+ B cells and a lower percentage of CD79b+ cells were found in PLN of the immunized dogs compared with dogs of Group WT. Immunohistochemical investigation showed no parasites in the PLN of immunized dogs whereas there were parasites in the PLN of 60% of dogs infected with L. infantum WT. In this study, the immunophenotypic profile of mononuclear cells of the immunized dogs correlates with cellular immunity.
Dexamethasone, a common medication used in the treatment regimen of glioblastoma, has broad inhibitory effects on the immune responses. Here, in an in vitro study, we examined the effects of piroxicam, a potent substitute for dexamethasone, on peripheral blood mononuclear cells (PBMCs) co-cultured with two glioblastoma cell lines, U-87 MG and A-172 cells. MTT assay was used to determine the proliferation of PBMCs treated with piroxicam, or dexamethasone. In addition, to evaluate the effects of drugs on the cell cycle distribution, DNA content per cell was analyzed in PBMCs and A-172 cell lines using flow cytometry. Oxidative parameters, including superoxide dismutase-3 (SOD3) activity and total anti-antioxidant capacity, lactate dehydrogenase (LDH) activity, as well as IFN-γ and TGF-β levels were measured in PBMCs alone or in the presence of cell lines using ELISA. Unlike dexamethasone, piroxicam showed a protective effect on PBMCs against both glioblastoma cell lines. Furthermore, while dexamethasone reduced the proliferation of PBMCs, piroxicam had no adverse effect on the proliferation. Cell cycle analysis showed a reduction in the G2/M phase in piroxicam-treated A-172 cells. Additionally, dexamethasone limited the cell cycle progression by increasing the fraction of PBMCs in G0/G1. Interestingly, after co-culturing piroxicam-treated PBMCs with cell lines, a remarkable rise in the LDH activity was observed. Although not significant, piroxicam partially decreased TGF-β levels in both cell lines. Our findings suggested a protective effect of piroxicam, but not dexamethasone, on PBMCs against inhibitory mechanisms of two glioblastoma cell lines, U-87 and A-172 cells.
Immunometabolism is an emerging field in tumor immunotherapy. Understanding the metabolic competition for access to the limited nutrients between tumor cells and immune cells can reveal the complexity of the tumor microenvironment and help develop new therapeutic approaches for cancer. Recent studies have focused on modifying the function of immune cells by manipulating their metabolic pathways. Besides, identifying metabolic events, which affect the function of immune cells leads to new therapeutic opportunities for treatment of inflammatory diseases and immune-related conditions. According to the literature, metabolic pathway such as glycolysis, TCA cycle, and fatty acid metabolism, significantly influence the survival, proliferation, activation, and function of immune cells and thus regulate immune responses. In this paper, we reviewed the role of metabolic processes and major signaling pathways involving in T-cell regulation and T-cell responses against tumor cells. Moreover, we summarized the new therapeutics suggested to enhance anti-tumor activity of T cells through manipulating metabolic pathways.
Background: Dexamethasone, a common medication used in the treatment regimen of glioblastoma, has broad inhibitory effects on the immune responses. Here in an in vitro study, we examined the effects of piroxicam, a potent substitute for dexamethasone, on peripheral blood mononuclear cells (PBMCs) co-cultured with U-87 MG glioblastoma cell line.Methods: MTT assay was used to determine the proliferation of PBMCs treated with piroxicam, or dexamethasone. In addition, oxidative parameters, including superoxide dismutase-3 (SOD3) activity and total antioxidant capacity (TAC), lactate dehydrogenase (LDH) activity, as well as IFN-γ and TGF-β levels were measured in PBMCs alone or the presence of U-87 MG cells using ELISA. Results: unlike dexamethasone, piroxicam showed a protective effect on PBMCs against U-87 MG cell line. Furthermore, while dexamethasone reduced the proliferation of PBMCs, piroxicam had no adverse effect on the proliferation. LDH activity was also lower in piroxicam-treated U-87 MG cells; interestingly, after co-culturing piroxicam-treated PBMCs with U-87 MG cell line, a remarkable rise in the LDH activity was observed. Although not significant, piroxicam partially decreased TGF-β levels in U-87 cells. Conclusion: our findings suggested a protective effect of piroxicam, but not dexamethasone, on PBMCs against inhibitory mechanisms of the U-87 MG cell line.
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