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To investigate the inflammatory mechanism of nasal instillation of fine particulate matter (PM)on hippocampal tissue injury in mice. Thirty C57BL/6J mice were randomly divided into 3 groups(n=10):control group, low-dose group, high-dose group. The nasal instillation doses of PM in the low-dose group and the high-dose group were 1.5 mg/kg BW and 7.5 mg/kg BW, respectively, and the control group was given saline with an equal volume. Saline was sprayed once every other time for 12 times. The serum levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) were determined by ELISA method. HE staining and electron microscopy were used to observe the pathological changes and ultrastructure of lung tissue and hippocampus. The inflammatory cytokine levels in hippocampus were detected by antibody chip technique. There was no significant effect of PM nasal instillation on serum TNF-α, IL-1β and IL-6 levels (P＞0.05), and there was no obvious pathological changes in lung tissue structure. In hippocampus, low-dose and high-dose PM exposure could lead to disordered neuronal arrangement in the hippocampal CA3 region, and there were neurological changes around the neuron cells and ultrastructural changes such as edema around small blood vessels. Compared with the control group, the levels of inflammatory cytokines such as CX3CL1, CSF2 and TECK in the low-dose group were increased significantly (P ＜0.05), while sTNFR1 was decreased significantly (P＜0.05); the inflammatory factors CX3CL1, CSF2, and TCA-3 were significantly increased in the high-dose group (P＜0.05), while leptin, MIG, and FASLG were significantly decreased (P＜0.05). Nasal instillation of PM can induce tissue damage in the hippocampus of mice, and its mechanism of action may be the olfactory brain pathway. The increasing of TNF-α and IL-6 and the decreasing of sTNFR1 and FASLG may be involved in inflammatory mechanisms.
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Objective To analysis the expression levels of inflammatory cytokines in patients with cluster headache during headache attack period and intermittent period using antibody chips to explore the role of inflammatory cytokines in the pathogenesis of cluster headache. Methods Blood samples from 6 patients with cluster headache were collected during headache attack period and intermittent period. Samples were then centrifugated and stored at - 80 degrees refrigerator. Samples were further labeled with biotin and reacted with antibody chips against 40 major inflammatory cytokines. The target proteins were conjugated with streptomycin antibody labeled with infrared fluorescent agent, and signals were transformed to images by Licor-odyssey scanner. Results In pairwise comparisons, the levels of some inflammatory cytokines were significantly increased during attacks compared to intermittent period including interleukin-1β(44.18 vs. 68.46, P<0.05), interleukin-6(23.08 vs. 36.40, P<0.05), interleukin-8(151.87 vs. 328.12, P<0.05), interleukin-13(23.93 vs. 38.87, P<0.05), monoeyte chemoattraetant protein (454.80 vs. 725.75, P<0.05) and macrophage inflammatory protein-1β (265.08 vs. 515.74, P<0.05). Conclusion Inflammatory cytokines may play an important role in the pathogenesis of cluster headache. However, the mechanism needs further investigation.
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Objective To investigate the role of inflammatory cytokines in the pathogenesis of chronic non-bacterial prostatitis/chronic pelvic pain syndrome (CAP/CPPS) patients. Methods The 38 cases with CAP/CPPS patients (18 cases of CAP and 20 cases of CPPS) and 20 cases of healthy controls were selected. The differential expressions of 40 kinds of inflammatory cytokines were detec-ted by antibody arrays in prostate fluid. Results The inflammatory cytokines which increased more than 1.5 times expression have been found. There were seven kinds in CAP including monocyte che-moattractant protein (MCP)-1, solution tumor necrosis factor receptor Ⅱ(s TNF R Ⅱ), platelet-de-rived growth faetor-BB (PDGF-BB), interleukin (IL)-β, IL-11、IL-6、MCP-2 and five kinds in CPPS groups including MCP-1、PDGF-BB、MCP-2、s TNF R Ⅱ、It-11 respectively, compared with healthy control group. The cluster analysis results showed that protein expression of Monocyte chemoattrac-tant protein 1 (MCP-1)and platelet-derived growth factor BB (PDGF-BB) were significantly increased in CAP (3.47 and 2.07 times) and CPPS (2.25 and 2.19 times) compared with healthy control group and were the final polymerization of inflammatory cytokines. The protein expression of interleukin 1 β (IL-1 β), MCP-1 and soluble tumor necrosis factor Ⅱ (s TNF R Ⅱ) in CAP group was increased more than 1.85,1.55,1.67 times compared with CPPS group. Conclusions Elevated expression of inflammatory cytokines may play an important role in the course of CAP/CPPS disease. The extent of the inflammatory response of CAP was higher than CPPS. The inflammatory factors of MCP-1 and PDGF-BB could serve as a novel diagnostic marker.
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Objective To investigate the expression of inflammatory cytokines in patients with severe sepsis by using an antibody chip.Methods Twelve patients with severe sepsis and other 10 patients whose age and gender were matehed were enrolled in this study.Proteins from patients were labeled with biotin.The biotin-labeled proteins reaeted with antibody chips,on which there were antibodies of 40 major inflammatory cytokines.The target proteins were conjugated with streptomycin antibody labeled by horseradish peroxidase(HRP),and signals were imaged by laser scanner.Results In comparison with control group,the serum levels of inflammatory eytokines ineluding pro-and anti-inflammatory cytokines,ehemokines and certain eytokines receptors were notably increased,while expression of anti-inflammatory interleukin(IL)-2,-4,-13,-15 was remarkably decreased in sepsis group.Conclusions Excess inflammatory response and imbalance of pro-and anti-inflammatory eytokines were presented in the eourse of severe sepsis.