Laboratory of Liver, Pancreas and Motility (HIPAM), Department of Experimental Medicine, Facultad de Medicina-Universidad Nacional Autónoma de México (UNAM), México.
J Neurogastroenterol Motil. 2010 Oct;16(4):363-73. doi: 10.5056/jnm.2010.16.4.363. Epub 2010 Oct 30.
The irritable bowel syndrome (IBS) is a complex disorder in which psychosocial, cultural and biological factors, interact. Recent knowledge in the pathophysiology of IBS, seem to combine issues such as a low grade inflammation or immune activation and dysbiosis that can trigger or exacerbate IBS. On the other hand, stress mediated through the hypothalamic-pituitary-adrenal axis can produce motility abnormalities that can modify the microbiota as well, with the subsequent immune activation in the mucosa and stimulation of nerve terminals, generating symptoms of IBS. Also, we speculate that, stress, dysbiosis or an underlying genetic predisposition, may increase the epithelial permeability leading to a contact between pathogens-associated molecular patterns and toll-like receptors in the deeper layers of the gut, developing a host immunity response and IBS generation. We believe that the role of toll-like receptors in IBS and elucidating the communication processes between the immune and the nervous system, warrant future research.
肠易激综合征(IBS)是一种复杂的疾病,其中社会心理、文化和生物因素相互作用。IBS 病理生理学的最新知识似乎将低度炎症或免疫激活和微生物失调等问题结合在一起,这些问题可能会引发或加重 IBS。另一方面,通过下丘脑-垂体-肾上腺轴介导的应激会产生运动异常,也可以改变微生物群,随后在黏膜中产生免疫激活,并刺激神经末梢,产生 IBS 症状。此外,我们推测,应激、微生物失调或潜在的遗传易感性可能会增加上皮通透性,导致病原体相关分子模式与肠道深层 Toll 样受体接触,从而产生宿主免疫反应和 IBS。我们认为,Toll 样受体在 IBS 中的作用以及阐明免疫和神经系统之间的通信过程,值得进一步研究。