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Abstract

Metal ions are integral parts of pro- as well as eukaryotic cell homeostasis. Escherichia coli proved a valuable in vitro model organism to elucidate essential mechanisms involved in uptake, storage, and export of metal ions. Given that E. coli Nissle 1917 is able to overcome murine colonization resistance, we generated several E. coli Nissle 1917 mutants with defects in zinc, iron, copper, nickel, manganese homeostasis and performed a comprehensive survey of the impact of metal ion transport and homeostasis for E. coli colonization capacities within the murine intestinal tract. Seven days following peroral infection of conventional mice with E. coli Nissle 1917 strains exhibiting defined defects in zinc or iron uptake, the respective mutant and parental strains could be cultured at comparable, but low levels from the colonic lumen. We next reassociated gnotobiotic mice in which the microbiota responsible for colonization resistance was abrogated by broad-spectrum antibiotics with six different E. coli K12 (W3110) mutants. Seven days following peroral challenge, each mutant and parental strain stably colonized duodenum, ileum, and colon at comparable levels. Taken together, defects in zinc, iron, copper, nickel, and manganese homeostasis do not compromise colonization capacities of E. coli in the murine intestinal tract.

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We have previously shown that Arcobacter butzleri induces intestinal, extra-intestinal, and systemic immune responses in perorally infected gnotobiotic IL-10−/− mice in a strain-dependent fashion. Here, we present a comprehensive survey of small and large intestinal expression profiles of inflammatory and regulatory mediators as well as of the matrix-degrading gelatinases MMP-2 and MMP-9 following murine A. butzleri infection. Gnotobiotic IL-10−/− mice were infected with A. butzleri strains CCUG 30485 or C1 of human and chicken origin, respectively. At day 6 following A. butzleri infection, mucin-2 mRNA, an integral part of the intestinal mucus layer, was downregulated in the colon, whereas TNF and IL-23p19 mRNA were upregulated in the ileum. Furthermore, IFN-γ, IL-17A, IL-1β, and IL-22 mRNA were upregulated in both colonic and ileal ex vivo biopsies at day 6 post strain CCUG 30485 infection. These changes were accompanied by downregulated colonic MMP-9 levels, whereas both MMP-2 and MMP-9 mRNA were upregulated in the ileum. In conclusion, these data indicate that A. butzleri infection induces changes in the expression of genes involved in pro-inflammatory and regulatory immune responses as well as in tissue degradation.

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MM Vickerman KE Carey 1983 Survival and implantation of Escherichia coli in the intestinal tract Infect Immun

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-inflammatory effects of NAP treatment were not restricted to the intestinal tract, given that extra-intestinal and even systemic collateral damages of inflammation could be alleviated [ 11 , 12 ]. This prompted us to elucidate potential immune-modulatory actions of

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The processes of digestion in the avian gastrointestinal tract depend on sophisticated control systems that co-ordinate secretion of digestive juices and movement of the luminal contents. In the current study, the distribution of serotonin-, gastrin-, glucagon- and somatostatin-immunoreactive endocrine cells was investigated by immunocytochemical methods in the intestinal tract of the goose. The number of cells immunoreactive for each antiserum was evaluated in different regions of the intestinal tract. Serotonin-, glucagon- and somatostatin-immunoreactive endocrine cells were seen throughout the intestinal tract, but somatostatin-immunoreactive cells were not detected in the colon of the goose. Gastrin-immunoreactive cells were detected only in the duodenum, jejunum and colon mucosa. It is concluded that the distribution pattern of the entero-endocrine cells in the goose is similar to that of most of the mammalian and other poultry species.

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Abstract  

The rare-earth elements are very suitable multiple particulate markers for the investigation of matter flow in the gastro-intestinal tract of animals by means of the indicator activation method. A rapid determination of cerium and samarium in biological samples is possible with the aid of a 14 MeV neutron generator. The activity of139mCe has to be corrected for the interferences of28Al and143mSm. For the determination of samarium the radionuclides155Sm and153Sm are used. In order to increase the specific activity of these nuclides, which are produced mainly by means of nuclear reactions with thermal neutrons, the samples are irradiated inside a polyethylene moderator block. The deviation from the linearity of the calibration curve for samarium is discussed.

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European Journal of Microbiology and Immunology
Authors: Gangadhararao Appana, Dipankar Das, Maroudam Veerasami, Ramachandran Lakshmikanthan Senthilkumar, Munishkumar Durishetty, B. Ramalakshmi, Vijay Bahekar, Falguni Mukherjee, Dev Chandran, P. Uday Kumar, B. Sesikeran, and Dr. Villuppanoor Alwar Srinivasan Ph.D.

Abstract

A male cattle calf was detected as subclinically and naturally infected with Mycobacterium avium subspecies paratuberculosis (MAP) by a series of antemortem and postmortem tests. The MAP infection was identified by strong antibody and cell-mediated immune (CMI) response by a commercial ELISA kit and an intradermal Johnin test, respectively, in the initial antemortem examination. The antemortem status of the calf was further confirmed by MAP-specific interferon gamma (IFN-γ) response. For detection of IFN-γ response, MAP-specific IFN-γ release assays (IGRAs): (a) immuno capture ELISA (IC-ELISA) and (b) ELISPOT was employed. In addition, the presence of intracellular cytokine IFN-γ was detected by flow cytometry. For all cytokine assays, MAP-specific recombinant antigens HSP65 and 35 kDa were employed to overcome the poor sensitivity and specificity resulting from the use of Johnin, the crude protein purified derivative of MAP. Postmortem examination of the MAP-infected/suspected cattle calf did not reveal any pathognomonic gross lesions in the gastro-intestinal tract. Histopathological examination of multiple organs showed the presence of epithelioid cells/macrophages and edematous lesions in the mesenteric lymph nodes suggestive of MAP; however, no granulomas were observed in the intestinal tract. The necropsy samples of rectum and mesenteric lymph nodes were positive for isolation of MAP by culture in the BACTEC™ MGIT™ 960 system, and acid fast bacilli were demonstrated by fluorescence microscopy confirming the infection. Due to differential and complex expression patterns of MAP antigens reported in literature, a combination of assays such as those based on IGRAs and antibody detection is essential. Therefore, the current experimental evidence confirms the efficacy of the approach adopted. However, further studies will be needed to understand the optimal combination MAP-specific antigens for use in IGRAs or antibody assays that can be used for detecting MAP infection in every stage of the disease.

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European Journal of Microbiology and Immunology
Authors: Marie E. Alutis, Ursula Grundmann, André Fischer, Ulrike Hagen, Anja A. Kühl, Ulf B. Göbel, Stefan Bereswill, and Markus M. Heimesaat

Matrix metalloproteinases (MMP)-2 and -9 (also referred to gelatinases-A and -B, respectively) are upregulated in the inflamed gut of mice and men. We recently demonstrated that synthetic gelatinase blockage reduced large intestinal pro-inflammatory immune responses and apoptosis following murine Campylobacter (C.) jejuni infection. In order to address which gelatinase mediates C. jejuni-induced immune responses, gnotobiotic MMP-2−/−, MMP-9−/−, and wildtype (WT) mice were generated by broadspectrum antibiotic treatment and perorally infected with C. jejuni strain 81-176. The pathogen stably colonized the murine intestinal tract irrespective of the genotype but did not translocate to extra-intestinal compartments. At days 8 and 14 postinfection (p.i.), less pronounced colonic histopathological changes were observed in infected MMP-2−/− mice, less distinct epithelial apoptosis, but more epithelial proliferation in both MMP-2−/− and MMP-9−/− mice, as compared to WT controls. Reduced immune responses in gelatinase- deficient mice were characterized by lower numbers of effector as well as innate and adaptive immune cells within the colonic mucosa and lamina propria. The expression of IL-22, IL-18, IL-17A, and IL-1β mRNA was higher in the colon of MMP-2−/− as compared to WT mice. In conclusion, both MMP-2 and MMP-9 are differentially involved in mediating C. jejuni-induced intestinal immunopathology.

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European Journal of Microbiology and Immunology
Authors: Marie E. Alutis, Ursula Grundmann, Ulrike Hagen, André Fischer, Anja A. Kühl, Ulf B. Göbel, Stefan Bereswill, and Markus M. Heimesaat

Increased levels of the matrix metalloproteinases (MMPs)-2 and -9 (also referred to gelatinase-A and -B, respectively) can be detected in the inflamed gut. We have recently shown that synthetic gelatinase blockage reduces colonic apoptosis and pro-inflammatory immune responses following murine Campylobacter (C.) jejuni infection. In order to dissect whether MMP-2 and/or MMP-9 is involved in mediating C. jejuni-induced immune responses, infant MMP-2-/-, MMP-9-/-, and wildtype (WT) mice were perorally infected with the C. jejuni strain B2 immediately after weaning. Whereas, at day 2 postinfection (p.i.), fecal C. jejuni B2 loads were comparable in mice of either genotype, mice expelled the pathogen from the intestinal tract until day 4 p.i. Six days p.i., colonic MMP-2 but not MMP-9 mRNA was upregulated in WT mice. Remarkably, infected MMP-2-/- mice exhibited less frequent abundance of blood in feces, less distinct colonic histopathology and apoptosis, lower numbers of effector as well as innate and adaptive immune cells within the colonic mucosa, and higher colonic IL-22 mRNA levels as compared to infected WT mice. In conclusion, these results point towards an important role of MMP-2 in mediating C. jejuni-induced intestinal immunopathogenesis.

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Extraintestinal pathogenic Escherichia coli (ExPEC) isolates of animals and man are known to carry specific virulence associated genes. The intestinal tract, it is primarily colonized by various strains of commensal E. coli but it may include ExPEC as well. Here we aimed to assess possible genetic and evolutionary linkages between extraintestinal pathogenic and intestinal (commensal) E. coli of poultry. For that purpose we analysed 71 ExPEC isolates, and 40 intestinal isolates assumed to be commensal E. coli (IntEC), from dead chickens and turkey poults for 26 virulence related genes. Although the two groups shared several virulence determinants the genes pic, papC, and cdtIV were exclusively present in ExPEC and further five genes (colV, iss, kpsM, tsh and iutA), were significantly more frequent among ExPEC. Phylogenetic backgrounds of ExPEC and of IntEC isolates indicated significant differences. A 40% of ExPEC belonged to phylogroup A primarily containing strains of serogroup O78. Phylogroup D contained ExPEC strains of serogroups O53 (2 strains) and O115 (5 strains) characterized by the cdt-IV genes, suggesting the existence of new clones of avian ExPEC in phylogenetic group D. On the other hand, a 42.5% of IntEC belonged to phylogroup B1 with diverse serogroups. Our data provide insight into the clonal evolution of avian ExPEC especially in phylogenetic groups A and D, resulting avian ExPEC with similarities to human ExPEC.

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