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伤寒热作为急性难治性支气管哮喘发作的触发因素。

Typhoid fever as a triggering factor in acute and intractable bronchial asthma attack.

作者信息

Surachmanto Eko E, Datau E A

机构信息

Department of Internal Medicine, Siloam International Hospitals. Karawaci, Indonesia.

出版信息

Acta Med Indones. 2013 Oct;45(4):312-20.

PMID:24448337
Abstract

Typhoid fever is an enteric infection caused by Salmonella typhi. In Indonesia, typhoid fever is endemic with high incidence of the disease. In daily practice we frequently have patients with bronchial asthma, and it is becoming worse when these patients get typhoid fever. After oral ingestion, Salmonella typhi invades the the intestine mucosa after conducted by microbial binding to epithelial cells, destroying the microfold cells (M cell) then passed through the lamina propria and detected by dendritic cells (DC) which express a variety of pathogen recognition receptors on the surfaces, including Toll-Like Receptor (TLR). expressed on macrophages and on intestinal epithelial cells inducing degradation of IB, and translocation of NF-B (Nuclear Factor-Kappa Beta). This process initiates the induction of pro-inflammatory gene expression profile adhesion molecules, chemokines, adhesion molecules, and other proteins that induce and perpetuate the inflammation in host cells then will induce acute ant intractable attack of bronchial asthma. The role of typhoid fever in bronchial asthma, especially in persons with acute attack of bronchial asthma, is not well understood. In this article, we will discuss the role of typhoid fever in the bronchial asthma patients which may cause bronchial asthma significantly become more severe even triggering the acute and intractable attack of bronchial asthma. This fact makes an important point, to treat completely the typhoid fever in patients with bronchial asthma.

摘要

伤寒热是由伤寒沙门氏菌引起的一种肠道感染。在印度尼西亚,伤寒热呈地方性流行,发病率很高。在日常临床实践中,我们经常会遇到支气管哮喘患者,而当这些患者感染伤寒热时,病情会加重。口服后,伤寒沙门氏菌通过与上皮细胞的微生物结合侵入肠道黏膜,破坏微褶细胞(M细胞),然后穿过固有层,并被在表面表达多种病原体识别受体的树突状细胞(DC)检测到,这些受体包括Toll样受体(TLR)。其在巨噬细胞和肠道上皮细胞上表达,诱导IκB降解以及核因子κB(NF-κB)易位。这一过程启动了促炎基因表达谱的诱导,包括黏附分子、趋化因子、黏附分子以及其他诱导并维持宿主细胞炎症的蛋白质,进而会诱发支气管哮喘的急性难治性发作。伤寒热在支气管哮喘中的作用,尤其是在支气管哮喘急性发作患者中的作用,目前尚不清楚。在本文中,我们将探讨伤寒热在支气管哮喘患者中的作用,它可能会使支气管哮喘显著加重,甚至引发支气管哮喘的急性难治性发作。这一事实表明一个重要观点,即要彻底治疗支气管哮喘患者的伤寒热。

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