Immunotropic aspect of the Bacillus coagulans probiotic action

AbstractImmunotropic aspect of the Bacillus coagulans probiotic actionObjectiveCurrently, probiotics are increasingly used as the alternative to antibiotics as well as the preventive measures in humans. In particular, probiotics occupy a key position in the treatment of antibiotics-associated intestinal dysbiosis. A spore-forming microorganism lactobacillus Bacillus coagulans is one of the most promising probiotics. However, some of its pharmacological effects remain poorly understood.Aim.This study is aimed at investigation of the effect of Bacillus coagulans (Laktovit Forte) on the intestinal dysbiosis syndrome in mice caused by streptomycin against the background of cyclophosphamide-induced cellular immunodeficiency.Methods.Pharmacological method: mouse model in vivo with immunodeficiency caused by cyclophosphamide.Key findings.In mice with colitis caused by streptomycin treatment, the administration of Bacillus coagulans (Laktovit Forte medicinal product) resulted in an antidiarrheal effect, normalization of gastrointestinal motility, and prevention of the animals’ weight loss. Given the cyclophosphamide-induced immunosuppression and streptomycin-associated diarrhoea, the immunity was completely restored only under the action of Bacillus coagulans.Conclusions.According to all parameters, Bacillus coagulans has been proved to be more effective as compared to the Linex Forte reference product containing lacto‐ and bifidobacteria.

Download Full-text

CYP4F18-Deficient Neutrophils Exhibit Increased Chemotaxis to Complement Component C5a

Journal of Immunology Research ◽

10.1155/2015/250456 ◽

2015 ◽

Vol 2015 ◽

pp. 1-10 ◽

Cited By ~ 5

Author(s):

Rachel Vaivoda ◽

Christine Vaine ◽

Cassandra Boerstler ◽

Kristy Galloway ◽

Peter Christmas

Keyword(s):

Weight Loss ◽

Mouse Model ◽

Immune Regulation ◽

Complement Component ◽

Wild Type ◽

Eicosanoid Synthesis ◽

Colonic Tissue ◽

Significant Difference

CYP4Fs were first identified as enzymes that catalyze hydroxylation of leukotriene B4(LTB4). CYP4F18 has an unusual expression in neutrophils and was predicted to play a role in regulating LTB4-dependent inflammation. We compared chemotaxis of wild-type andCyp4f18knockout neutrophils using anin vitroassay. There was no significant difference in the chemotactic response to LTB4, but the response to complement component C5a increased 1.9–2.25-fold in knockout cells compared to wild-type (P< 0.01). This increase was still observed when neutrophils were treated with inhibitors of eicosanoid synthesis. There were no changes in expression of other CYP4 enzymes in knockout neutrophils that might compensate for loss of CYP4F18 or lead to differences in activity. A mouse model of dextran sodium sulfate colitis was used to investigate the consequences of increased C5a-dependent chemotaxisin vivo, but there was no significant difference in weight loss, disease activity, or colonic tissue myeloperoxidase between wild-type andCyp4f18knockout mice. This study demonstrates the limitations of inferring CYP4F function based on an ability to use LTB4as a substrate, points to expanding roles for CYP4F enzymes in immune regulation, and underscores thein vivochallenges of CYP knockout studies.

Download Full-text

Abstract 495: Mouse Model of Mesenteric Ischemia Secondary to Vascular Calcification and Atherosclerosis

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/atvb.37.suppl_1.495 ◽

2017 ◽

Vol 37 (suppl_1) ◽

Author(s):

Konstantinos Damiris ◽

Filippo Romanelli ◽

Alexei Savinov ◽

José Luis Millan ◽

Jes Kuruvilla ◽

...

Keyword(s):

Weight Loss ◽

Mouse Model ◽

Mesenteric Ischemia ◽

Intestinal Ischemia ◽

Density Lipoprotein ◽

Body Weight Loss ◽

Goblet Cells ◽

Mesenteric Arteries ◽

Chronic Mesenteric Ischemia

Objective: Atherosclerosis is a leading cause of chronic mesenteric ischemia (CMI), defined as intestinal hypoperfusion resulting from stenosis of mesenteric arteries. Symptoms of CMI range from non-specific abdominal pain and weight loss to aversion of food resulting in cachexia. In this study we aim to define intestinal ischemia and its effects on gastrointestinal structure and function in an in vivo model of atherosclerosis. Hypothesis: Overexpression of tissue-nonspecific alkaline phosphatase (TNAP) under conditions of hypercholesterolemia in a mouse model will lead to atherosclerosis causing intestinal ischemia. Methods and Results: We have previously established that endothelial TNAP overexpression (eTNAP) results in calcification of medium-sized arteries including mesenteric. In this study eTNAP was combined with a point mutation in the low-density lipoprotein receptor ( ldlr ^WHC). When fed an atherogenic diet (Paigen’s diet, starting at 8 weeks of age), WHC-eTNAP mice developed acute body weight loss (>15% from baseline), whereas WHC mice continued to gain weight. Examination of the mesenteries of WHC-eTNAP demonstrated eccentric vascular remodeling and stiffening, as well as calcification of atherosclerotic plaques (n=4). Mesenteric arteries of WHC were not affected (n=3). WHC-eTNAP (n=2) mice developed extensive atherosclerosis of submucosal arterioles in the colon where most vessels were narrowed or occluded. Examination of the small intestine in WHC-eTNAP mice showed structurally distressed villi accompanied with an increase in goblet cells and fragmentation of the epithelial layer possibly reflecting cell death. The colon demonstrated loss of goblet cells and signs of denuding of the epithelium. Conclusion: Atherosclerosis induced by overexpression of TNAP causes occlusion of mesenteric arteries as well as structural pathology in the small and large intestine

Download Full-text