The aim of this study was to investigate the use of a standardized animal model subjected to antibiotic treatment, and the effects of this treatment on the course of dextran sodium sulphate (DSS)-induced colitis in mice. By decontamination with selective antibiotics and observation of pathogenesis of ulcerative colitis (UC) induced chemically by exposure of mice to various concentrations of DSS, we obtained an optimum animal PGF model of acute UC manifested by mucin depletion, epithelial degeneration and necrosis, leading to the disappearance of epithelial cells, infiltration of lamina propria and submucosa with neutrophils, cryptitis, and accompanied by decreased viability of intestinal microbiota, loss of body weight, dehydration, moderate rectal bleeding, and a decrease in the selected markers of cellular proliferation and apoptosis. The obtained PGF model did not exhibit changes that could contribute to inflammation by means of alteration of the metabolic status and the induced dysbiosis did not serve as a bearer of pathogenic microorganisms participating in development of ulcerative colitis. The inflammatory process was induced particularly by exposure to DSS and its toxic action on compactness and integrity of mucosal barrier in the large intestine. This offers new possibilities of the use of this animal model in studies with or without participation of pathogenic microbiota in IBD pathogenesis.

Alginite is a non-ore raw material arising by fossilization of accumulated organic (algae) and inorganic material, particularly clay, carbonates, quartz, and amorphous modification of silicic acid in the aqueous environment. Humic acids as a component of organic portion of alginite are known for very good buffering ability which allows them to stabilise pH throughout the digestion system of animals, stimulate receptors of the immune system in intestinal villi against pathogenic bacteria, and support proliferation and activity of beneficial bacteria (lactobacilli, bifidobacteria, and similar). Our investigations focused on the influence of a probiotic strain in combination with alginite on intestinal microenvironment of SPF mice infected with Salmonella Typhimurium. The 66 female mice (BALB/c) used in our study were divided to four experimental groups, control NC1, control NC2 (alginite), IC (alginite + Salmonella Typhimurium CCM 7205_NAL), LAB (Lact. reuteri CCM 8617 + alginite + Salm. Typhimurium CCM 7205_NAL). The group supplemented with Lact.reuteri CCM 8617 and alginite showed significant reduction in growth of Salm. Typhimurium in mice faeces at 24 and 72 h (P < 0.001) post infection. The supplementation of additives affected positively also nitrogen, enzymatic, hepatic and energy metabolism of mice. The demonstrable positive influence of additives alleviated the negative impact of Salm. Typhimurium infection on the morphology investigated in the jejunum and ileum of LAB group of mice. The livers of mice treated with both alginite and Lact.reuteri CCM 8617 showed marked reduction of overall inflammation, hepatocyte necrosis and size of typhoid nodules.

Inflammatory bowel disease (IBD) is a group of disorders causing inflammation in the digestive tract. Recent data suggest that dysbiosis may play a pivotal role in the IBD pathogenesis. As microbiome-based therapeutics that modulate the gut ecology have been proposed as a novel strategy for preventing IBD, the aim of presenting study was to evaluate the dextran sulphate sodium (DSS) rat model mainly in terms of microbial shifts to confirm its suitability for dysbiosis study in IBD. Acute colitis was induced using 5% DSS solution for seven days and rats were euthanized five days after DSS removal. The faecal/caecal microbiota was analyzed by next generation sequencing. Disease activity index (DAI) score was evaluated daily. Blood and colon tissue immunophenotyping was assessed by flow cytometry and histological, haematological, and biochemical parameters were also evaluated. The colitis induction was reflected in a significantly higher DAI score and changes in all parameters measured. This study demonstrated significant shifts in the colitis-related microbial species after colitis induction. The characteristic inflammation-associated microbiota could be detected even after a five day-recovery period. Moreover, the DSS-model might contribute to an understanding of the effect of different treatments on extraintestinal organ impairments. The observation that certain bacterial species in the gut microbiota are associated with colitis raises the question of whether these organisms are contributors to, or a consequence of the disease. Despite some limitations, we confirmed the suitability of DSS-induced colitis model to monitor microbial changes during acute colitis, in order to test attractive new microbiome-based therapies.

The present study investigated the effects of enterocin (Ent) M and sage extract alone and also in combination on the gut microflora, phagocytic activity, blood biochemistry, and morphometry of rabbits. Sixty-four rabbits (aged five weeks, M91 meatline, both sexes) were divided into three experimental groups: E (EntM; 50 µL/animal/day), S (sage; 10 µL/animal/day), and E + S (EntM + sage) groups and control group (C). The additives were administered in drinking water for a period of 21 days. Dietary supplementation of EntM and sage significantly reduced the coliforms (E: p < 0.001; S: p < 0.001; E + S: p < 0.001) in feces, while simultaneous addition of EntM and sage decreased enterococci (E + S: p < 0.0001), lactic acid bacteria (E + S: p < 0.01), and coagulase-positive staphylococci (E + S: p < 0.0001) in the appendix. Sage addition reduced HDL (S: p < 0.001) and LDL cholesterol (S: p < 0.001; E + S: p < 0.001), LDL/HDL ratio (S: p < 0.001; E + S: p < 0.01), and increased urea (S: p < 0.01; E + S: p < 0.001) and creatinine (S: p < 0.001; E + S: p < 0.001) in serum. EntM and sage application, alone or in combination, improve the jejunal morphometry (p < 0.0001) in rabbits.

Thymol concentrations in rabbit plasma, intestinal wall (IW) and faeces were detected, and the effects of thymol application and withdrawal on biochemical, antioxidant parameters and fatty acids (FA) in blood (B) and muscle (M) were studied. Forty-eight rabbits were divided into two experimental groups (control, C and with thymol 250-mg/kg feed, T). Thymol was administered for 21 days (TA) and withdrawn for seven days (TW). Thymol in plasma correlated with that in the IW (Spearman′s correlation coefficient (r_s) = −1.000, p = 0.0167, TA) and was detected in faeces (TA and TW). In TA alkaline phosphatase (p = 0.0183), cholesterol (p = 0.0228), malondialdehyde (p = 0.003), glutathione peroxidase (p = 0.0177) in B and lactate dehydrogenase (M, p = 0.0411) decreased; monounsaturated FA (p = 0.0104) and α-linolenic acid (p = 0.0227) in M increased. In TW urea (p = 0.0079), docosapentaenoic acid (p = 0.0069) in M increased; linoleic acid (p = 0.0070), ∑ n−6 (p = 0.0007) in M and triglycerides decreased (B, p = 0.0317). In TA and TW, the total protein (p = 0.0025 and 0.0079), creatinine (B; p = 0.0357 and 0.0159) and oleic acid (M; p = 0.0104 and 0.0006) increased. Thymol was efficiently absorbed from the intestine and demonstrated its biological activity in blood and the muscles.

This investigation was performed to assess the supplementation of probiotics on cytokine expression and lymphocyte subpopulation in Campylobacter coli challenged chickens. Thirty-six individuals were equally separated into four experimental treatments: C = untreated chickens, LB = probiotic control ( Lactobacillus fermentum ), Cc = Campylobacter -challenged control, LBCc = probiotic + Cc. All chicks were slaughtered and cecum samples were collected on day 4 postinfection. Gene expression analysis, using reverse transcription quantitative PCR (RT-qPCR), revealed significant differences in cytokine transcript expression between untreated and probiotic-treated chickens. In addition, flow cytometry was used to quantitate the levels of lymphocyte subpopulations. Principal component analysis showed that probiotic administration induced an overall downregulation of cytokine expression. C. coli exposure provoked a similar response to that of L. fermentum but to a lesser extent. Colonization of C. coli in the presence of the probiotic evoked a complex response with an upregulation of some type II cytokines, including interleukin IL-4 and IL-13, which could explain the increased presence of antibodies in both lamina propria and epithelium. Moreover, despite that the percentage of CD8 intraepithelial lymphocytes (IELs) was found to be higher, downregulation of proinflammatory cytokines IL-15, IL-16, and interferon γ was observed. This suggests that the detected CD8 are not effector cells but induced IELs, which release antimicrobial peptides, and are ready to be primed upon encountering antigen. These outcomes demonstrate that probiotic administration promotes a humoral response to a C. coli infection while dampening any potential inflammation mediated by effector T cells in 1-week-old chicks.