Abstract
Clinical studies have shown that probiotics influence gastrointestinal motility. However, the molecular mechanisms by which probiotic Lactobacillus modulates intestinal motility in traumatic brain injury (TBI) mouse model have not been explored. In the present study, we provided evidence showing that treatment of TBI mice with Lactobacillus acidophilus significantly improved the terminal ileum villus morphology, restored the impaired interstitial cells of Cajal (ICC) and the disrupted ICC networks after TBI, and prevented TBI-mediated inhibition of contractile activity in intestinal smooth muscle. Mechanistically, the decreased concentration of MLCK, phospho-MLC20 and phospho-MYPT1 and increased concentration of MLCP and PKC were observed after TBI, and these events mediated by TBI were efficiently prevented by Lactobacillus acidophilus application. These findings may provide a novel mechanistic basis for the application of Lactobacillus acidophilus in the treatment of TBI.
Highlights
Traumatic brain injury (TBI) occurs when an external force traumatically injures the brain
We found that treatment of mice with Lactobacillus acidophilus efficiently improved the contractile properties of intestinal smooth muscle, which were impaired by TBI
We found that protein kinase C (PKC)/myosin light chain kinases (MLCK)/ MLC signaling pathway could play an important role in Lactobacillus acidophilus-mediated improvement of contractile properties of intestinal smooth muscle after TBI
Summary
Traumatic brain injury (TBI) occurs when an external force traumatically injures the brain. TBI is a major cause of death and disability worldwide. A World Health Organization study estimated that 70–90% of patients suffer a mild TBI, a substantial number of patients suffer a severe TBI [1]. Increasing evidence shows that TBI can lead to several physiologic complications including gastrointestinal dysfunction [2]. Traumatic brain injury causes a delayed but significant decrease in intestinal contractile activity, which is associated with disturbances in food intake and inadequate nutrition [3]. Development of optimal treatment strategies to improve intestinal motility has important clinical significance
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