Toxoplasma gondii causes death and plastic alteration in the jejunal myenteric plexus

AIM:To assess the effects of ME-49 Toxoplasma gondii(T.gondii) strain infection on the myenteric plexus and external muscle of the jejunum in rats.METHODS:Thirty rats were distributed into two groups:the control group(CG)(n = 15) received 1 m L of saline solution orally, and the infected group(IG)(n=15)inoculated with 1 m L of saline solution containing500 oocysts of M-49 T.gondii strain orally.After 36 d of infection,the rats were euthanized.Infection with T.gondii was confirmed by blood samples collected from all rats at the beginning and end of the experiment.The jejunum of five animals was removed and submitted to routine histological processing(paraffin)for analysis of external muscle thickness.The remaining jejunum from the others animals was used to analyze the general population and the NADH-diaphorase,VIPergic and nitrergic subpopulations of myenteric neurons;and the enteric glial cells(S100-IR).RESULTS:Serological analysis showed that animals from the IG were infected with the parasite.Hypertrophy affecting jejunal muscle thickness was observed in the IG rats(77.02±42.71)in relation to the CG(51.40±12.34),P<0.05.In addition,31.2%of the total number of myenteric neurons died(CG:39839.3±5362.3;IG:26766.6±2177.6;P<0.05);hyperplasia of nitrergic myenteric neurons was observed(CG:7959.0±1290.4;IG:10893.0±1156.3;P<0.05);general hypertrophy of the cell body in the remaining myenteric neurons was noted[CG:232.5(187.2-286.0);IG:248.2(204.4-293.0);P<0.05];hypertrophy of the smallest varicosities containing VIP neurotransmitter was seen(CG:0.46±0.10;IG:0.80±0.16;P<0.05)and a reduction of 25.3%in enteric glia cells(CG:12.64±1.27;IG:10.09±2.10;P<0.05)was observed in the infected rats.CONCLUSION:It was concluded that infection with oocysts of ME-49 T.gondii strain caused quantitative and plastic alterations in the myenteric plexus of the jejunum in rats.

What are the effects of proton pump inhibitors on the small intestine?

Generally, proton-pump inhibitors(PPIs) have great benefit for patients with acid related disease with less frequently occurring side effects. According to a recent report, PPIs provoke dysbiosis of the small intestinal bacterial flora, exacerbating nonsteroidal anti-inflammatory drug-induced small intestinal injury.Several meta-analyses and systematic reviews have reported that patients treated with PPIs, as well as post-gastrectomy patients, have a higher frequency of small intestinal bacterial overgrowth(SIBO) compared to patients who lack the aforementioned conditions.Furthermore, there is insufficient evidence that these conditions induce Clostridium difficile infection. At this time, PPI-induced dysbiosis is considered a type of SIBO. It now seems likely that intestinal bacterial flora influence many diseases, such as inflammatory bowel disease, diabetes mellitus, obesity, nonalcoholic fatty liver disease, and autoimmune diseases.When attempting to control intestinal bacterial flora with probiotics, prebiotics, and fecal microbiota transplantation, etc., the influence of acid suppression therapy, especially PPIs, should not be overlooked.

The prolonged effect of glucagon-like peptide 2 pretreatment on growth performance and intestinal development of weaned piglets

Background： Glucagon-like peptide 2 （GLP-2） is a potent epithelium-specific intestinal growth factor. The aim of this study was to demonstrate the prolonged effect of GLP-2 on the growth performance of weaned piglets. Forty piglets weaned at the age of 28 d with an average BW of 6.8 ＋ 0.4 kg were assigned to four treatments： （i） non- challenged control; （ii） LPS-challenged control; （iii） LPS ＋ low GLP-2; and （iv） LPS ＋ high GLP-2. Piglets in groups （i）, （ii）, and （iv） were s.c. injected with PBS supplemented with human [Gly2]GLP-21-34 at doses of 0, 2 and 10 nmol/kg BW per day for seven consecutive days. BW, gain：feed ratio （G：F）, and plasma GLP-2 levels were determined on d 0 7, and 14 after weaning. Piglets were challenged with i.p. administration of Escherichia coil lipopolysaccharide （LPS） at a dose of 100 pg/kg on d 14 to induce intestinal damage. Twenty-four hours later, intestinal tract samples were collected to assess intestinal morphology and quantify enzyme activity. Results： Plasma GLP-2 levels decreased after weaning, but in the high GLP-2 group, plasma GLP-2 was maintained on d 7 and even increased to a level higher than the preweaning level on d ]4 （P 〈 0.05）. High GLP-2 treatment significantly increased the duodenal, jejunal and ileal weight, as well as the gross weight of the small intestine （SI）, and the SI weight index （P 〈 0.05）. LPS caused villous atrophy and disrupted intestinal morphology in the duodenum, jejunum and ileum. GLP-2 also significantly increased the villus height and the villus height/crypt depth ratio （VCR） of the duodenum, jejunum, and ileum （P 〈 0.05）. Histological examination revealed that in GLP-2-treated groups, the integrity of the villus was maintained, and the villus was protected against LPS-induced damage. GLP-2 significantly increased the activity of alkaline phosphatase （AKP）, y-glutamyltranspeptidase （y-G-i-）, and pancreatic lipase in the duodenum and jejunum （P 〈 0.05）. GLP-2 treatment also significantly increased the average daily gain （ADG） and G：F of piglets at 0 to 7, 7 to 14, as well as 0 to14 d （P 〈 0.05）, resulting in a significant increase of final 8W in high GLP-2 pigs （P = 0.016）. Conclusions： Exogenous GLP-2 improved the growth of weaned piglets and protected them against LPS-induced intestinal damage. These effects may be due to the ability of GLP-2 to promote the secretion of endogenous GLP-2 to stimulate the small intestinal development.