Coccidiosis has a negative economic impact on the commercial poultry industry, and probiotics are beneficial bacteria that aid in maintaining healthy gut microflora. We hypothesized that probiotic administration would positively affect gut morphology and increase IgG secretion during an Eimeria challenge, which was evaluated by measuring total chicken IgG and gut morphology (villus height, villus width, villus surface area, crypt depth, villus height to crypt depth ratio and lamina propria thickness). On day-of-hatch, broilers were placed into floor pens with 50 percent pine shavings and 50 percent used litter. The broilers were exposed to Eimeria oocysts via the feed on day 14 and challenged on day 36. On days 6, 22, 36, and 43, tissue samples from the intestine were collected for morphological evaluation, and blood samples were taken to quantify chicken IgG from serum. Data were measured using a factorial ANOVA and main effect means were deemed significant at P ≤ 0.05. In cases where significant interactions were observed, data was subjected to a one-way ANOVA. All means were separated using a Duncan’s Multiple Range Test. On day 6 in the duodenum, a significant interaction was observed regarding vaccination and probiotic administration (Coccivac®-B, Intervet/Schlering-Plough Animal Health/Merck and Co., Inc., Whitehouse Station, NJ). Villus height to crypt depth ratio decreased in ionophore treated birds compared to control birds in the duodenum and lower ileum on day 6, 36, and 43. Villus crypt depth in vaccinated birds decreased in the duodenum after the challenge. On day 43, the ionophore treated birds had less villus height and surface area compared to control and vaccinated birds, while lamina propria thickness increased in the duodenum, and non probiotic birds had longer villi than probiotic birds. On day 22, vaccinated birds had significantly increased chicken IgG levels compared to the control and ionophore birds, and the non probiotic birds had significantly increased IgG secretion compared to probiotic fed birds. On day 36, the ionophore birds had significantly increased levels of IgG compared to the control birds, which could also support that the ionophore delayed exposure to the parasite. These results suggest that gut morphology and humoral immunity are affected by probiotic administration, coccidiosis vaccination, ionophore application and Eimeria challenge. Both the day 43 morphology results and day 36 chicken IgG results for the ionophore treated birds demonstrates that ionophore administration delays exposure of the avian gut to invasive coccidia. More research is necessary to evaluate how probiotics influence coccidiosis vaccination and humoral immunity, so that probiotics may be used to improve the effectiveness of coccidiosis vaccination and to evaluate if probiotics aid in ameliorating the effects of an Eimeria infection.

Abstract In order to determine whether antigens prepared from adult intestine of Angiostrongylus cantonensis have potential to induce a protective immunity in the rodent hosts, somatic antigens extracted from male and female adults as well as gut antigens isolated from female adults were used to immunize rats against A. cantonensis infection. A 14% reduction in L5 recorvery from brain as well as a 15% reduction in adult recovery from pulmonary artery were achieved in the immunized rats when compared with the control group after infection with 50 larvae. The length of worms recovered from immunized rats was shorter than that in other groups. The larvae recovered from fecal materials in immunized rats were also reduced. In cell proliferation test, the stimulation index of gut antigens increased with times of immunization and exhibited the highest values. However, serum IgG titers were not correlated with protective immune responses. A 84 kDa protein contained in all antigen preparations was recognized by immune serum against gut antigens. Strong positive reactions were detected by indirect immunofluorescent assay in the internal musculature of the body, gut and reproductive tract wall and gut lumen. The composition of gut antigens was similar to that of gut membrane proteins. Immune sera recognized several major gut proteins were also appeared on gut membrane proteins. Further studies are required to provide evidence that gut membrane proteins play in the protective immune response against A. cantonensis infections, including the 84 kDa protein.

Metabolic syndrome is a disease affecting 25% of North America’s population causing strain on the medical systems. With diet and exercise, genetics, environment, and the gut microbiota all being targeted as potential causes of the disease, there is a lack of consensus on the exact aetiology and pathophysiology. With improved methods in bioinformatic sequencing of faecal bacterial DNA in recent years, our research indicates that a dysbiosis in the gut microbiome is both necessary and sufficient in causing immunological changes in the host in order for the development of metabolic syndrome, T1Ds, and T2Ds. Specifically, our data indicates these shifts in microbiota occur prior to the onset of disease, and produce the disease regardless of diet and genetics. The findings in the current study indicate that future research towards manipulating the gut microbiota to prevent disease, as well as using the faecal bacteria as a screening tool should be pursued.

Univ., Diss.--Amsterdam, 2006. / Zsfassung in niederländ. Sprache.

Univ., Diss.--Mannheim, 1998.

Universiẗat, Diss.--Köln, 2000.

Heidelberg, Univ., Diss., 2006. / Online publiziert: 2008.

Bachelor-Arbeit Univ. St. Gallen, 2008.

Inflammatory bowel disease (IBD) is associated with an inappropriate immune response to the gut microbiota and disruption of intestinal homeostasis. IBD patients and experimental animal models have consistently shown alterations in the gut microbiota composition. However, these studies have mainly focused on faecal microbiota samples taken after the onset of inflammation and IBD establishment. The colonic microbiota inhabits both the gut lumen and the mucus layer covering the intestinal epithelium. Thus, information about mucus-resident microbiota is not necessarily conveyed in the routine microbiota analyses of faecal samples. To address potential changes in microbial composition and function before the onset of IBD, we compared both mucus and faecal microbiota in the mdr1a-/- spontaneous model of colitis over times that we histologically defined as before onset of colitis, during and after colitis onset. We showed that alterations in microbiota composition preceded the onset of intestinal inflammation and that these changes were evident in the mucus, but not in faeces. This altered microbiota composition was coupled with a reduced inner mucus layer, indicating a compromised mucus barrier prior to colitis development. Upon emergence of inflammation, compositional differences were found in both mucus and faecal microbial communities. Spatial segregation of microbiota with intestinal mucosa was also disrupted on disease onset which we hypothesise contributes to a more severe intestinal pathology. Therefore, our data indicate that microbial changes start locally in the mucus and then proceed to the faecal matter concomitantly with colitis development. Next, we examined whether microbial gene functional potential and endogenous metabolite profiles followed alterations in gut microbiota taxonomic composition. Our findings showed that the microbial gene content was similar between mdr1a-/- mice and wild-type littermate controls, demonstrating stability of the gut microbiome at the face of ensuing gut inflammation. In further support of these findings, urinary metabolite analysis revealed that metabolite profiles were unaffected by intestinal inflammation. Metabolites previously reported to change in IBD were similar between mdr1a-/- and wild-type mice at stages preceding and during inflammation. We also found that changes in metabolite profiles did not correlate with colitis scores. However, metabolite changes could discriminate mdr1a-/- mice from wild-type controls, suggesting they could have value in predicting risk of IBD with a potential clinical use in at least a subset of individuals with MDR1A polymorphisms. To assess whether changes in antimicrobial proteins (AMPs) accounted for observed differences in mucus microbiota composition, we also investigated the expression of regenerating islet-derived protein 3 γ (Reg3γ), angiogenin 4 (Ang4), β-defensin 1 and resistin-like molecule beta (Relm-β) in the colon. We found similar levels of these AMPs as well as IgA-producing plasma cells between mdr1a-/- and wild-type mice, suggesting that other factors contribute to alterations in microbiota composition. Overall, our data indicate that the mdr1a-/- is a good model of colitis, as it enables us to look at pre-clinical changes in the gut microbiota. This work suggests the importance of mucus sampling for sensitive detection of microbiota changes. Furthermore, metabolite profiling may be a helpful way to discriminate genetic susceptibility to disease.

Objective: To determine the variations in the composition of the intestinal microbiota in asymptomatic children infected with Helicobacter pylori in comparison with children without the infection. Results: Children infected with H. pylori doubled their probability of presenting 3 of 9 genera of bacteria from the gut microbiota, including: Proteobacteria (p = 0.008), Clostridium (p = 0.040), Firmicutes (p = 0.001) and Prevotella (p = 0.006) in comparison to patients without the infection. We performed a nutritional assessment and found that growth stunting was statistically significantly higher in patients infected with H. pylori (p = 0.046). / Revisión por pares / Revisión por pares