Mechanical model of steady-state and inflammatory conditions in patients with relapsing polychondritis: A review.
Mechanical model of steady-state and inflammatory conditions in patients with relapsing polychondritis: A review.
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DOI：
10.1097/md.0000000000028852
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发表时间：
2022-02-25
期刊：
影响因子：
1.6
通讯作者：
Suzuki N
中科院分区：
文献类型：
--
作者：
Shimizu J;Suzuki N
复发性多囊炎是一种多系统炎症性疾病，被认为与免疫异常有关。RP患者中报告了T辅助细胞1型相关细胞因子增加。与健康人相比，RP患者外周血单个核细胞中调节性T细胞因子白细胞介素（IL）-10的mRNA表达增加，而促炎性细胞因子IL 1 β和IL 6的mRNA表达减少。在体外用丝裂原刺激后，RP患者IL 10 mRNA表达降低，IL 1 β和IL 6 mRNA表达升高。这种免疫细胞的基因表达从抗炎到促炎特征的短时间动态变化可能与RP患者的“复发”病程相关。呼吸系统受累患者外周血单个核细胞IL 1 β mRNA表达与血清基质金属蛋白酶（MMP-3）浓度呈正相关。在无呼吸道受累的患者中未发现这种正相关。在宏基因组分析中，发现肠道微生物的组成发生了变化，这表明微生物代谢物如短链脂肪酸可能会影响患者的T细胞反应。本文就RP相关炎症分子之间的关系作一综述。这些数据支持了一个假设，即RP患者的稳态和炎症之间的免疫状况是不同的。
Relapsing polychondritis (RP) is a multisystem inflammatory disorder, considered to associate with immune aberration. Increased T helper type-1 cell-related cytokines were reported in RP patients. mRNA expressions of a regulatory T cell cytokine interleukin (IL)-10 increased, whereas pro-inflammatory cytokines IL1β and IL6 mRNA expressions decreased in freshly isolated peripheral blood mononuclear cells of RP patients compared with those in healthy individuals. Upon in vitro stimulation with mitogen, IL10 mRNA expressions decreased, and IL1β and IL6 mRNA expressions increased in RP patients. This short-time dynamic change of gene expressions from anti-inflammatory to pro-inflammatory features of immune cells may be associated with the “relapsing” disease course of patients with RP. IL1β mRNA expressions of peripheral blood mononuclear cells exhibited positive correlations with serum matrix metalloproteinase (MMP)-3 concentrations in patients with respiratory involvement. Such positive correlation was not found in those without respiratory involvement. In a metagenomic analysis, an altered composition of gut microbes was found, suggesting that microbe metabolites such as short-chain fatty acids may affect T cell responses of the patients. In this review, the relationships among RP-related inflammatory molecules were summarized. The data support a hypothesis that the immune conditions are different between steady-state and inflammation in RP patients.