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151.
蛋白酶3(proteinase 3,PR3)是中性粒细胞分泌的主要丝氨酸蛋白酶之一,其生物学功能广泛,不仅能降解多种组织蛋白,还可通过加工细胞因子、受体等调控炎症反应,与慢性炎症性疾病如血管炎性肉芽肿病、慢性阻塞性肺疾病、肺囊肿性纤维症的发生发展密切相关,可能作为疾病防治靶点.本文主要综述了PR3的生物学功能及其在疾病中的可能作用机制,期望为相关疾病的防治提供新的思路. 相似文献
152.
Yuka Kobayashi Norikazu Kiguchi Yohji Fukazawa Fumihiro Saika Takehiko Maeda Shiroh Kishioka 《The Journal of biological chemistry》2015,290(20):12603-12613
Peripheral neuroinflammation caused by activated immune cells can provoke neuropathic pain. Herein, we investigate the actions of macrophages and T cells through glucocorticoid-induced tumor neurosis factor receptor ligand (GITRL) and its receptor (GITR) in neuropathic pain. After partial sciatic nerve ligation (PSL) in enhanced green fluorescent protein (eGFP) chimeric mice generated by the transplantation of eGFP+ bone marrow cells, eGFP+ macrophages, and T cells markedly migrated to the injured site after PSL. Administration of agents to deplete macrophages (liposome-clodronate and Clophosome-ATM) or T cells (anti-CD4 antibody and FTY720) could suppress PSL-induced thermal hyperalgesia and tactile allodynia. The expression levels of co-stimulatory molecules GITRL and GITR were increased on infiltrating macrophages and T cells, respectively. The perineural injection of a GITRL neutralizing antibody that could inhibit the function of the GITRL-GITR pathway attenuated PSL-induced neuropathic pain. Additionally, the induction of inflammatory cytokines and the accumulation of GITR+ T cells in the injured SCN were abrogated after macrophage depletion by Clophosome-ATM. In conclusion, GITRL expressed on macrophages drives cytokine release and T cell activation, resulting in neuropathic pain via GITR-dependent actions. The GITRL-GITR pathway might represent a novel target for the treatment of neuropathic pain. 相似文献
153.
《Trends in microbiology》2015,23(6):367-375
154.
Yu-Ching Tsai Wei-Hsin Hsiao Sheng-Hsiang Lin Hsiao-Bai Yang Hsiu-Chi Cheng Wei-Lun Chang Cheng-Chan Lu Bor-Shyang Sheu 《Journal of biomedical science》2015,22(1)
Background
Gastric cancer exhibits familial clustering, and gastric cancer familial relatives (GCF) tend to present with corpus-predominant gastritis and precancerous lesions as SPEM or IM after H. pylori infection. The study determined whether the children of gastric cancer patients (GCA) had genomic single nucleotide polymorphisms (SNPs) predisposed to the gastric precancerous lesions as spasmolytic polypeptide-expressing metaplasia (SPEM) or intestinal metaplasia (IM).Results
There were 389 family relatives of 193 non-cardiac GCA and 173 duodenal ulcer patients (DU), received blood sampling for DNA collection. The differences of the risk alleles of SNPs in the ITGA5, ITGB1, IL-10, COX-2, RUNX3, and TFF2 genes were compared between 195 children of GCA and 143 DU. The children of GCA had higher allele frequencies of ITGA5-1160 T-carrier (P = 0.006, OR[95% CI] = 2.2[1.2-4]), ITGB1-1949 A-carrier (P = 0.047; OR[95% CI] = 2.8[1.4-5.3]), ITGB1 + 31804 C-carrier (P = 0.013; OR[95% CI] = 4.7[1.7-13.0]), IL-10-592 AA (P = 0.014; OR[95% CI] = 2.3[1.4-4.0]) and COX-2-1195 G-carrier (P = 0.019; OR[95% CI] = 1.7[0.9-3.2]) than DU. The combined genotype with ITGA5-1160/ITGB1-1949/ITGB1 + 31804 as T/A/C carriers and COX-2-1195/IL-10-592 as G-carrier/AA was more prevalent in the children of GCA than in DU (P < 1×10−4), and predisposed with a 5.3-fold risk of getting SPEM in the H. pylori-infected children of GCA (P = 0.016). Such risk of getting SPEM increased to 112 folds, if combined with RUNX3 + 492/TFF2-308 as A-carrier/CC in this limited study scale (P = 1×10−4).Conclusions
The SNPs of ITGA5-1160/ITGB1-1949/ ITGB1 + 31804 as T/A/C carriers and COX-2-1195/IL-10-592 as G-carrier/AA, or more specific to combine RUNX3 + 492/TFF2-308 as A-carrier/CC shall be host factor predisposing to gastric cancer during H. pylori infection, and serve as marker to identify high-risk subjects for H. pylori eradication.Electronic supplementary material
The online version of this article (doi:10.1186/s12929-015-0121-7) contains supplementary material, which is available to authorized users. 相似文献155.
过氧化物酶体增殖物激活受体γ(peroxisome proliferator-activated receptorγ,PPAR-γ)通路是调节替换活化的(alternatively activated)M2型巨噬细胞极化的中心环节.姜黄素是PPAR-γ的天然激动剂,有着良好的抗炎作用.本研究通过建立巨噬细胞株的体外炎症模型,用姜黄素及PPAR-γ的特异性抑制剂GW9662对其进行干预,观察巨噬细胞株极化状态的改变.结果显示,姜黄素可以促使巨噬细胞向M2型极化,当特异性抑制PPAR-γ通路后,姜黄素促进巨噬细胞向M2型极化的作用受到抑制.结果表明,姜黄素可能是通过激动PPAR-γ通路促使巨噬细胞向M2型极化,为进一步研究姜黄素的抗炎机制及治疗慢性低度炎症相关的代谢性疾病提供了一个新的思路. 相似文献
156.
Enhanced Expression of Indoleamine 2,3‐Dioxygenase in Helicobacter pylori‐Infected Human Gastric Mucosa Modulates Th1/Th2 Pathway and Interleukin 17 Production 下载免费PDF全文
157.
158.
Neutrophil extracellular trap cell death requires both autophagy and superoxide generation 总被引:1,自引:0,他引:1
Remijsen Q Vanden Berghe T Wirawan E Asselbergh B Parthoens E De Rycke R Noppen S Delforge M Willems J Vandenabeele P 《Cell research》2011,21(2):290-304
Neutrophil extracellular traps (NETs) are extracellular chromatin structures that can trap and degrade microbes. They arise from neutrophils that have activated a cell death program called NET cell death, or NETosis. Activation of NETosis has been shown to involve NADPH oxidase activity, disintegration of the nuclear envelope and most granule membranes, decondensation of nuclear chromatin and formation of NETs. We report that in phorbol myristate acetate (PMA)-stimulated neutrophils, intracellular chromatin decondensation and NET formation follow autophagy and superoxide production, both of which are required to mediate PMA-induced NETosis and occur independently of each other. Neutrophils from patients with chronic granulomatous disease, which lack NADPH oxidase activity, still exhibit PMA-induced autophagy. Conversely, PMA-induced NADPH oxidase activity is not affected by pharmacological inhibition of autophagy. Interestingly, inhibition of either autophagy or NADPH oxidase prevents intracellular chromatin decondensation, which is essential for NETosis and NET formation, and results in cell death characterized by hallmarks of apoptosis. These results indicate that apoptosis might function as a backup program for NETosis when autophagy or NADPH oxidase activity is prevented. 相似文献
159.
160.
Marie Billaud Diana Dahan Roger Marthan Jean-Pierre Savineau Christelle Guibert 《Respiratory research》2011,12(1):30