Cell sub-journal's latest research: a little happier, healthier stomach!

Guide: To always be happy, the gastrointestinal tract will be a little more comfortable Oh
neurotransmitters can change gastrointestinal physiology (GI) by regulating intestinal smooth muscle contraction, blood flow under the mucous membrane, barrier function, immune response, and the secretion of chloride and potassium, neurotransmitters also change the behavior of bacteria, and affect the toxicity of many pathogensserotonin (also known as serotonin) is a monoamine neurotransmitter that controls human emotions, appetite and sleep, mainly in the gastrointestinal tract (GI) synthesis, and then secreted into the tube cavity, and then eliminated by the 5-serotonin transporter protein SERTprevious studies have shown that many pathogens affect the signalconductiof of serotonin in the gastrointestinal tract, but the effect of serotonin on the pathogenesis of bacteria is still unknown, researchers from the University of Texas Southwestern Medical Center published their latest findings on serotonin in CellHostand Microbe, finding thatserotonin can reduce intestinal harm by de-phosphorizing the transcription factors of the toxic gene of the fire-fighting pathogen, reducing the expression of the toxic gene of pathogens such as Ecoli (EHEC) and rodent Citrate (EHEC mouse model)EHEC is progened in the human colon and can lead to hemorrhagic diarrhea and hemolytic uremia syndrome (HUS)The toxicity of EHEC is determined by the formation of adhesion and disappearance (AE) damage to Shiga toxin and intestinal epithelial cellsAE lesions, on the other hand, require the disappearance of intestinal epithelial cells (LEE) disease-causing island (PI) containing gene expressionthe researchers first tested serotonin in the colon tissue of mice and found that when microorganisms were present, the concentration of serotonin decreasedThen from transcription and protein levels, respectively, physiological concentration of serotonin presence, serotonin 5-serotonin will inhibit the encoding of all LEE gene transcription activation factors of the expression of the ler gene, which in turn led to the LEE disease island gene espA, espB, eae and tir expression decreasedA study of the transcription group affecting EHEC by serotonin 5-serotonin found that 13 genes were raised, 55 were lowered, and the lowered genes were mainly LEE genesAll this shows that serotonin reduces the expression of the toxic gene, the LEE disease-causing island gene, and the formation of AE damageserotonin reduces LEE gene expression and the formation of AE damage in ethnosome Ecoli
previous studies have shown that neurotransmitter epinephrine and norepinephrine can be perceived by the histine sensor kinase (HKs) bound by bacterial membranes, and HK can be activated or inactivated by phosphorylation and dephosphosphinizationThe researchers found that the only expression in the transcription group data of the HONG that was significantly regulated by serotonin was cpxA, part of the CpxRA two-component systemUsing genetic and biochemical phenotype analysis, cpxA was found to sense the neurotransmitter serotonin in mammalsSince CpxRA regulation occurs at the transcription level of the first gene in the LEE1 manipulator, which affects the transcription of all LEE genes, serotonin inhibits the expression of the LEE gene in EHEC by blocking the activation of CpxACpxA is a bacterial serotonin sensor
and the researchers then used the modified mouse model of sepsis (which produces Shiga toxin) as an invivite model to study the pathogenesis of EHEC, as SERT can remove 5-from the intestinal mucosa Serotonin, compared to wild type, the symptoms of EHEC and pathogenic gene expression in mice with SERT mutation model were reduced, the amount of bacillus tituatary in feces and colon decreased, and the mortality rate was also reduced when infected with bacillus bacillatAt the same time, the expression level of the LEE disease-causing island gene in colon tissue in mutant model mice was also reduced in line with previous studiesThe researchers also used fluoxetine to inhibit SERT in pharmacology, and the test ingested on mice with SERT mutant modelsThese data show that the accumulation of serotonin in the intestines reduces the expression of the toxic gene in the rodent Citrate, resulting in a decrease in the host's sensitivity to the pathogenin mice infected, the accumulation of tube serotonin reduces the toxicity of Bacillus citratein short, the study found that 5-serotonin can reduce the damage to the human gastrointestinal tract by inhibiting the expression of EHEC and the rodent Citalistemia toxicity geneSo,to always be happy, the gastrointestinal tract will be a little more comfortable oh