Activation of chloride channels and promotion of bowel movements by heat-killed Bifidobacterium longum CLA8013.

IF 2.5 Q3 MICROBIOLOGY
Bioscience of microbiota, food and health Pub Date : 2024-01-01 Epub Date: 2024-03-15 DOI:10.12938/bmfh.2023-084
Yutaka Makizaki, Mana Kishimoto, Yoshiki Tanaka, Hiroshi Ohno
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引用次数: 0

Abstract

Constipation is strongly associated with the deterioration of quality of life (QOL), and patients with constipation desire clear spontaneous defecation without the feeling of incomplete evacuation, rather than improved defecation frequency. The use of common osmotic or stimulant laxatives has not been shown to lead to a satisfactory improvement of bowel movements. In addition, softening of stools by increasing their water content has been reported to increase the frequency of spontaneous defecation and improve hard stools, straining during defecation, and abdominal symptoms, such as abdominal bloating, thereby leading to improvement of QOL deterioration caused by constipation. Thus, the present study screened bacterial strains in vitro using intestinal epithelial T84 cells, aiming to identify one that activates chloride channels involved in water secretion into the intestinal tract. As a result, the conditioned medium of Bifidobacterium longum CLA8013 was found to induce ion transport. Also, this effect was suppressed by cystic fibrosis transmembrane conductance regulator (CFTR) (inh)-172, a CFTR chloride channel inhibitor. Furthermore, both live and heat-killed CLA8013 similarly induced ion transport, suggesting that bacterial cell components are responsible for the effect. In addition, the administration of heat-killed CLA8013 to loperamide-induced constipation rats resulted in an increase in fecal water content and promoted defecation. These results suggest that the active components in CLA8013 act on CFTR chloride channels in the intestinal tract, promote water secretion into the intestinal tract, and soften stools, thereby promoting bowel movements.

热杀死的长双歧杆菌 CLA8013 激活氯离子通道并促进肠道蠕动
便秘与生活质量(QOL)的下降密切相关,便秘患者希望排便通畅,没有排便不尽的感觉,而不是排便次数增多。使用普通的渗透性或刺激性泻药并不能令人满意地改善排便情况。此外,有报道称,通过增加粪便的含水量来软化粪便可增加自发排便的频率,改善硬便、排便时用力以及腹胀等腹部症状,从而改善便秘导致的 QOL 恶化。因此,本研究利用肠上皮 T84 细胞在体外筛选细菌菌株,旨在找出一种能激活参与向肠道分泌水分的氯离子通道的细菌。结果发现,长双歧杆菌 CLA8013 的条件培养基能诱导离子转运。此外,囊性纤维化跨膜传导调节因子(CFTR)(inh)-172(一种 CFTR 氯离子通道抑制剂)也抑制了这种效应。此外,活体和热杀灭的 CLA8013 同样诱导离子转运,这表明细菌细胞成分是产生这种效应的原因。此外,给洛哌丁胺诱导的便秘大鼠服用热杀灭的 CLA8013 会导致粪便含水量增加并促进排便。这些结果表明,CLA8013 中的活性成分可作用于肠道中的 CFTR 氯离子通道,促进肠道分泌水分,软化粪便,从而促进排便。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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CiteScore
6.20
自引率
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