PDF(Pubmed)
Abstract：
Cold-inducible RNA-binding protein (CIRP) is a damage-associated molecular pattern that plays a critical role in triggering inflammatory responses. It remains unknown whether CIRP is strongly associated with bacterial load, inflammatory response, and mortality in sepsis model. Pneumonia was induced in specific pathogen-free 8-9-week old male rats by injecting bacteria via puncture of the tracheal cartilage. The expressions of CIRP and proinflammatory cytokines [tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-1β] in lung tissues, alveolar macrophages (AMs), plasma, and bronchoalveolar lavage fluid (BALF) were determined by reverse transcription-polymerase chain reaction, western blotting, and enzyme-linked immunosorbent assay. The numbers of bacteria recovered from the lungs were correlated with the bacterial loads injected and mortality. The expressions of CIRP increased sharply as the bacterial loads increased in the lung tissues and AMs. The amounts of TNF-α, IL-6 and IL-1β proteins synthesized were dependent on the bacterial load in the lung tissues. Releases of CIRP, TNF-α, IL-6, and IL-1β increased with the bacterial load in the blood plasma. The proteins confirmed similar patterns in the BALF. CIRP was strongly associated with the releases of TNF-α, IL-6, and IL-1β in the lung tissues, blood plasma, and BALF, and showed a close correlation with mortality. CIRP demonstrated a strong association with bacterial load, which is new evidence, and close correlations with proinflammatory cytokines and mortality of pneumonia in rats, suggesting that it might be an interesting pneumonic biomarker for monitoring host response and predicting mortality, and a promising target for immunotherapy.
摘要：
冷诱导RNA结合蛋白（CIRP）是一种损伤相关的分子模式，在触发炎症反应中起着关键作用。尚不清楚CIRP是否与细菌负荷密切相关，炎症反应，脓毒症模型中的死亡率。通过气管软骨穿刺注射细菌，在无特定病原体的8-9周龄雄性大鼠中诱发肺炎。CIRP和促炎细胞因子[肿瘤坏死因子-α（TNF-α），肺组织中的白细胞介素-6（IL-6）和IL-1β]，肺泡巨噬细胞（AM），等离子体,和支气管肺泡灌洗液（BALF）通过逆转录-聚合酶链反应测定，西方印迹,和酶联免疫吸附测定。从肺中回收的细菌数量与注射的细菌负荷和死亡率相关。随着肺组织和AMs中细菌负荷的增加，CI-RP的表达急剧增加。TNF-α，合成的IL-6和IL-1β蛋白依赖于肺组织中的细菌负荷。CIRP的版本，TNF-α,IL-6和IL-1β随着血浆中细菌负荷的增加而增加。这些蛋白质证实了BALF中的相似模式。CIRP与TNF-α的释放密切相关，肺组织中的IL-6和IL-1β，血浆,和BALF,与死亡率密切相关。CIRP与细菌负荷有很强的相关性，这是新的证据,与促炎细胞因子和大鼠肺炎死亡率密切相关，这表明它可能是监测宿主反应和预测死亡率的有趣的肺炎生物标志物，和免疫疗法的一个有希望的目标。
