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铜绿假单胞菌对重塑呼吸道上皮的黏附

Pseudomonas aeruginosa adherence to remodelling respiratory epithelium.

作者信息

de Bentzmann S, Roger P, Puchelle E

机构信息

INSERM U314, CHR Maison Blanche, Reims, France.

出版信息

Eur Respir J. 1996 Oct;9(10):2145-50. doi: 10.1183/09031936.96.09102145.

Abstract

Pseudomonas aeruginosa is an opportunistic organism, which frequently colonizes the respiratory tract of patients with impaired host defence. In cystic fibrosis (CF) patients, this pathogen causes a progressive destructive bronchitis and bronchiolitis and is responsible for high mortality. Normal respiratory epithelium is protected against bacteria via mucus and mucociliary clearance. Alteration of mucociliary clearance and of glycosylation of mucins in CF facilitates the access of bacteria to the underlying airway epithelial cells. Intact respiratory epithelium does not bind P. aeruginosa, whereas injured respiratory epithelium is highly susceptible to P. aeruginosa adherence. We found that the high affinity of respiratory epithelium, from CF and non-CF sources, for P. aeruginosa, during the wound repair process is related to the apical expression of asialo ganglioside M1 (aGM1). The affinity of repairing respiratory epithelium for P. aeruginosa is time-dependent, and is related to transient apical expression of aGM1 at the surface of repairing respiratory epithelial cells. CF respiratory epithelial cells apically express more aGM1 residues with relation to an increased affinity for P. aeruginosa than non CF cells. High epithelial damage followed by repair represents a major cause of P. aeruginosa adherence to airway epithelium in cystic fibrosis. However, P. aerurignosa adherence and colonization are not restricted to cystic fibrosis disease and P. aeruginosa pneumonia may also occur in severely immunocompromised patients, suggesting that epithelial injury and decreased host-response favour the colonization of the airways by P. aeruginosa.

摘要

铜绿假单胞菌是一种机会致病菌,常定殖于宿主防御功能受损患者的呼吸道。在囊性纤维化(CF)患者中,这种病原体可导致进行性破坏性支气管炎和细支气管炎,并导致高死亡率。正常呼吸道上皮通过黏液和黏液纤毛清除作用抵御细菌。CF患者黏液纤毛清除功能及黏蛋白糖基化改变,有利于细菌接触下层气道上皮细胞。完整的呼吸道上皮不结合铜绿假单胞菌,而受损的呼吸道上皮对铜绿假单胞菌黏附高度敏感。我们发现,在伤口修复过程中,CF和非CF来源的呼吸道上皮对铜绿假单胞菌的高亲和力与去唾液酸神经节苷脂M1(aGM1)的顶端表达有关。修复中的呼吸道上皮对铜绿假单胞菌的亲和力具有时间依赖性,且与修复中的呼吸道上皮细胞表面aGM1的短暂顶端表达有关。与非CF细胞相比,CF呼吸道上皮细胞顶端表达更多aGM1残基,对铜绿假单胞菌的亲和力增加。严重上皮损伤后修复是CF患者气道上皮铜绿假单胞菌黏附的主要原因。然而,铜绿假单胞菌的黏附和定殖并不局限于囊性纤维化疾病,严重免疫功能低下患者也可能发生铜绿假单胞菌肺炎,这表明上皮损伤和宿主反应降低有利于铜绿假单胞菌在气道定殖。

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