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A Commensal Helicobacter sp. of the Rodent Intestinal Flora Activates TLR2 and NOD1 Responses in Epithelial Cells  [PDF]
Nadia Chaouche-Drider, Maria Kaparakis, Abdulgader Karrar, Maria-Isabel Fernandez, Letitia A. M. Carneiro, Jér?me Viala, Ivo Gomperts Boneca, Anthony P. Moran, Dana J. Philpott, Richard L. Ferrero
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0005396
Abstract: Helicobacter spp. represent a proportionately small but significant component of the normal intestinal microflora of animal hosts. Several of these intestinal Helicobacter spp. are known to induce colitis in mouse models, yet the mechanisms by which these bacteria induce intestinal inflammation are poorly understood. To address this question, we performed in vitro co-culture experiments with mouse and human epithelial cell lines stimulated with a selection of Helicobacter spp., including known pathogenic species as well as ones for which the pathogenic potential is less clear. Strikingly, a member of the normal microflora of rodents, Helicobacter muridarum, was found to be a particularly strong inducer of CXC chemokine (Cxcl1/KC, Cxcl2/MIP-2) responses in a murine intestinal epithelial cell line. Time-course studies revealed a biphasic pattern of chemokine responses in these cells, with H. muridarum lipopolysaccharide (LPS) mediating early (24–48 h) responses and live bacteria seeming to provoke later (48–72 h) responses. H. muridarum LPS per se was shown to induce CXC chemokine production in HEK293 cells stably expressing Toll-like receptor 2 (TLR2), but not in those expressing TLR4. In contrast, live H. muridarum bacteria were able to induce NF-κB reporter activity and CXC chemokine responses in TLR2–deficient HEK293 and in AGS epithelial cells. These responses were attenuated by transient transfection with a dominant negative construct to NOD1, and by stable expression of NOD1 siRNA, respectively. Thus, the data suggest that both TLR2 and NOD1 may be involved in innate immune sensing of H. muridarum by epithelial cells. This work identifies H. muridarum as a commensal bacterium with pathogenic potential and underscores the potential roles of ill-defined members of the normal flora in the initiation of inflammation in animal hosts. We suggest that H. muridarum may act as a confounding factor in colitis model studies in rodents.
Identification of NF-κB Modulation Capabilities within Human Intestinal Commensal Bacteria
Omar Lakhdari,Julien Tap,Fabienne Béguet-Crespel,Karine Le Roux,Tomas de Wouters,Antonietta Cultrone,Malgorzata Nepelska,Fabrice Lefèvre,Jo l Doré,Hervé M. Blottière
Journal of Biomedicine and Biotechnology , 2011, DOI: 10.1155/2011/282356
Abstract: The intestinal microbiota plays an important role in modulation of mucosal immune responses. To seek interactions between intestinal epithelial cells (IEC) and commensal bacteria, we screened 49 commensal strains for their capacity to modulate NF-κB. We used HT-29/kb-seap-25 and Caco-2/kb-seap-7 intestinal epithelial cells and monocyte-like THP-1 blue reporter cells to measure effects of commensal bacteria on cellular expression of a reporter system for NF-κB. Bacteria conditioned media (CM) were tested alone or together with an activator of NF-κB to explore its inhibitory potentials. CM from 8 or 10 different commensal species activated NF-κB expression on HT-29 and Caco-2 cells, respectively. On THP-1, CM from all but 5 commensal strains stimulated NF-κB. Upon challenge with TNF-α or IL-1β, some CM prevented induced NF-κB activation, whereas others enhanced it. Interestingly, the enhancing effect of some CM was correlated with the presence of butyrate and propionate. Characterization of the effects of the identified bacteria and their implications in human health awaits further investigations.
A Multi-Omic View of Host-Pathogen-Commensal Interplay in Salmonella-Mediated Intestinal Infection  [PDF]
Brooke L. Deatherage Kaiser, Jie Li, James A. Sanford, Young-Mo Kim, Scott R. Kronewitter, Marcus B. Jones, Christine T. Peterson, Scott N. Peterson, Bryan C. Frank, Samuel O. Purvine, Joseph N. Brown, Thomas O. Metz, Richard D. Smith, Fred Heffron, Joshua N. Adkins
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0067155
Abstract: The potential for commensal microorganisms indigenous to a host (the ‘microbiome’ or ‘microbiota’) to alter infection outcome by influencing host-pathogen interplay is largely unknown. We used a multi-omics “systems” approach, incorporating proteomics, metabolomics, glycomics, and metagenomics, to explore the molecular interplay between the murine host, the pathogen Salmonella enterica serovar Typhimurium (S. Typhimurium), and commensal gut microorganisms during intestinal infection with S. Typhimurium. We find proteomic evidence that S. Typhimurium thrives within the infected 129/SvJ mouse gut without antibiotic pre-treatment, inducing inflammation and disrupting the intestinal microbiome (e.g., suppressing Bacteroidetes and Firmicutes while promoting growth of Salmonella and Enterococcus). Alteration of the host microbiome population structure was highly correlated with gut environmental changes, including the accumulation of metabolites normally consumed by commensal microbiota. Finally, the less characterized phase of S. Typhimurium’s lifecycle was investigated, and both proteomic and glycomic evidence suggests S. Typhimurium may take advantage of increased fucose moieties to metabolize fucose while growing in the gut. The application of multiple omics measurements to Salmonella-induced intestinal inflammation provides insights into complex molecular strategies employed during pathogenesis between host, pathogen, and the microbiome.
Campylobacter jejuni induces transcytosis of commensal bacteria across the intestinal epithelium through M-like cells
Lisa D Kalischuk, Frances Leggett, G Douglas Inglis
Gut Pathogens , 2010, DOI: 10.1186/1757-4749-2-14
Abstract: C. jejuni induced translocation of non-invasive E. coli across confluent Caco-2 epithelial monolayers in the absence of disrupted transepithelial electrical resistance or increased permeability to a 3 kDa dextran probe. C. jejuni-infected monolayers displayed increased numbers of cells expressing the M cell-specific marker, galectin-9, reduced numbers of enterocytes that stained with the absorptive enterocyte marker, Ulex europaeus agglutinin-1, and reduced activities of enzymes typically associated with absorptive enterocytes (namely alkaline phosphatase, lactase, and sucrase). Furthermore, in Campylobacter-infected monolayers, E. coli were observed to be internalized specifically within epithelial cells displaying M-like cell characteristics.These data indicate that C. jejuni may utilize M cells to promote transcytosis of non-invasive bacteria across the intact intestinal epithelial barrier. This mechanism may contribute to the inflammatory immune responses against commensal intestinal bacteria commonly observed in IBD patients.Inflammatory bowel diseases (IBD) are chronic T cell-mediated diseases that are thought to result from the loss of immunologic tolerance towards commensal intestinal microorganisms [1]. Intestinal epithelial barrier dysfunction is proposed to be a primary factor contributing to IBD pathogenesis [2,3]. By facilitating the translocation of commensal bacteria across the intestinal barrier, dysfunction of the epithelium may enable the inappropriate activation of T lymphocytes that recognize and respond to constituents of the microbiota. Studies have shown that IBD patients exhibit increased rates of systemic endotoxemia [4], have higher amounts of bacterial DNA in their serum [5], and have exaggerated humoral immune responses to intestinal bacterial antigens [6-8], implying that bacterial antigens are able to translocate across the intestinal epithelium. Although several studies have observed elevated intestinal permeability ("leaky gut") and t
Comparison of Adhesin Genes and Antimicrobial Susceptibilities between Uropathogenic and Intestinal Commensal Escherichia coli Strains  [PDF]
Xiaohua Qin, Fupin Hu, Shi Wu, Xinyu Ye, Demei Zhu, Ying Zhang, Minggui Wang
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0061169
Abstract: The presence of adhesins is arguably an important determinant of pathogenicity for Uropathogenic Escherichia coli (UPEC). Antimicrobial susceptibilities were tested by agar dilution method, fifteen adhesin genes were detected by polymerase chain reaction, and multilocus sequence typing (MLST) was analyzed in 70 UPEC isolates and 41 commensal E. coli strains. Extended-spectrum β-lactamase (ESBL) was determined with confirmatory test. The prevalence of ESBL-producers in UPEC (53%, 37/70) was higher than the commensal intestinal isolates (7%, 3/41), and 97% (36/37) of the ESBL-producing UPEC harbored blaCTX-M genes. afa was present in 36% (10/28) UPEC isolates from recurrent lower urinary tract infection (UTI), and none in the acute pyelonephritis, acute uncomplicated cystitis or commensal strains (P<0.0001). papG was detected in 28% (20/70) of UPEC isolates, while 5% (2/41) of the commensal strains were papG positive (P = 0.0025), and the prevalence of papG was significantly higher in acute pyelonephritis group (71%) than the other two UTI groups (P<0.0001). The prevalence of flu, yqi, yadN and ygiL was significantly higher in UPEC isolates than in the commensal strains. ESBL-producing UPEC showed a lower prevalence of adhesin genes compared with non-ESBL-producing strains. The MLST profiles were different between UPEC and commensal strains, with ST131 (19%, 13/70) and ST10 (20%, 8/41) being the most common MLSTs, respectively. This study demonstrated that several adhesin genes were more prevalent in UPEC isolates than in commensal E. coli, and afa may be associated with recurrent lower UTI whereas papG is more frequently associated with acute pyelonephritis.
Like Will to Like: Abundances of Closely Related Species Can Predict Susceptibility to Intestinal Colonization by Pathogenic and Commensal Bacteria  [PDF]
B?rbel Stecher equal contributor ,Samuel Chaffron equal contributor,Rina K?ppeli equal contributor,Siegfried Hapfelmeier,Susanne Freedrich,Thomas C. Weber,Jorum Kirundi,Mrutyunjay Suar,Kathy D. McCoy,Christian von Mering,Andrew J. Macpherson,Wolf-Dietrich Hardt
PLOS Pathogens , 2010, DOI: 10.1371/journal.ppat.1000711
Abstract: The intestinal ecosystem is formed by a complex, yet highly characteristic microbial community. The parameters defining whether this community permits invasion of a new bacterial species are unclear. In particular, inhibition of enteropathogen infection by the gut microbiota ( = colonization resistance) is poorly understood. To analyze the mechanisms of microbiota-mediated protection from Salmonella enterica induced enterocolitis, we used a mouse infection model and large scale high-throughput pyrosequencing. In contrast to conventional mice (CON), mice with a gut microbiota of low complexity (LCM) were highly susceptible to S. enterica induced colonization and enterocolitis. Colonization resistance was partially restored in LCM-animals by co-housing with conventional mice for 21 days (LCMcon21). 16S rRNA sequence analysis comparing LCM, LCMcon21 and CON gut microbiota revealed that gut microbiota complexity increased upon conventionalization and correlated with increased resistance to S. enterica infection. Comparative microbiota analysis of mice with varying degrees of colonization resistance allowed us to identify intestinal ecosystem characteristics associated with susceptibility to S. enterica infection. Moreover, this system enabled us to gain further insights into the general principles of gut ecosystem invasion by non-pathogenic, commensal bacteria. Mice harboring high commensal E. coli densities were more susceptible to S. enterica induced gut inflammation. Similarly, mice with high titers of Lactobacilli were more efficiently colonized by a commensal Lactobacillus reuteri RR strain after oral inoculation. Upon examination of 16S rRNA sequence data from 9 CON mice we found that closely related phylotypes generally display significantly correlated abundances (co-occurrence), more so than distantly related phylotypes. Thus, in essence, the presence of closely related species can increase the chance of invasion of newly incoming species into the gut ecosystem. We provide evidence that this principle might be of general validity for invasion of bacteria in preformed gut ecosystems. This might be of relevance for human enteropathogen infections as well as therapeutic use of probiotic commensal bacteria.
Intestinal Microbiota Shifts towards Elevated Commensal Escherichia coli Loads Abrogate Colonization Resistance against Campylobacter jejuni in Mice  [PDF]
Lea-Maxie Haag, André Fischer, Bettina Otto, Rita Plickert, Anja A. Kühl, Ulf B. G?bel, Stefan Bereswill, Markus M. Heimesaat
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0035988
Abstract: Background The zoonotic pathogen Campylobacter jejuni is a leading cause of bacterial foodborne enterocolitis in humans worldwide. The understanding of immunopathology underlying human campylobacteriosis is hampered by the fact that mice display strong colonization resistance against the pathogen due to their host specific gut microbiota composition. Methodology/Principal Findings Since the microbiota composition changes significantly during intestinal inflammation we dissected factors contributing to colonization resistance against C. jejuni in murine ileitis, colitis and in infant mice. In contrast to healthy animals C. jejuni could stably colonize mice suffering from intestinal inflammation. Strikingly, in mice with Toxoplasma gondii-induced acute ileitis, C. jejuni disseminated to mesenteric lymphnodes, spleen, liver, kidney, and blood. In infant mice C. jejuni infection induced enterocolitis. Mice suffering from intestinal inflammation and C. jejuni susceptible infant mice displayed characteristical microbiota shifts dominated by increased numbers of commensal Escherichia coli. To further dissect the pivotal role of those distinct microbiota shifts in abrogating colonization resistance, we investigated C. jejuni infection in healthy adult mice in which the microbiota was artificially modified by feeding live commensal E. coli. Strikingly, in animals harboring supra-physiological intestinal E. coli loads, colonization resistance was significantly diminished and C. jejuni infection induced enterocolitis mimicking key features of human campylobacteriosis. Conclusion/Significance Murine colonization resistance against C. jejuni is abrogated by changes in the microbiota composition towards elevated E. coli loads during intestinal inflammation as well as in infant mice. Intestinal inflammation and microbiota shifts thus represent potential risk factors for C. jejuni infection. Corresponding interplays between C. jejuni and microbiota might occur in human campylobacteriosis. Murine models introduced here mimick key features of human campylobacteriosis and allow for further analysis of immunological and molecular mechanisms of C. jejuni – host interactions.
Antibiotic Resistance in Intestinal Commensal Bacteria Isolated from Faecal Samples from Pigs and Pig Farm Workers in Greece
Anastasios Minas,Evanthia Petridou,Eleftheria Bourtzi-Chatzopoulou,Vasilios Krikelis,Aggelos Papaioannou,Panagiotis Plageras
Research Journal of Biological Sciences , 2012,
Abstract: The increased antibiotic resistance of intestinal commensal bacteria of food-producing animals in the last decade due to the extensive use of antibiotics is a potential risk for human health. In the present study, the prevalence of antibiotic resistance of E. coli, E. faecalis and E. faecium isolated from faecal samples from fattening pigs and pig farm workers who are not in contact with animals (group A) and pig farm workers who are in direct contact with animals (group B) was determined. The resistance of the bacteria was assessed by the determination of Minimum Inhibitory Concentration (MIC) of each antibiotic used in the study by microdilution method. E. coli isolated from fattening pigs showed resistance to at least one antibiotic used in the study at 93.20%, from pig farm workers of group A at 60.19% and of group B at 41.74%. The isolates of E. faecalis from fattening pigs, pig farm workers of group A and pig farm workers of group B were resistant to at least one antibiotic used in the study at 73.78, 68.93 and 52.42%. The resistance of E. faecium isolated from the same groups was determined at 62.13, 52.43 and 44.66%. E. coli and Enterococci isolated from pigs showed high resistance to tetracyclines, sulfamethoxazone, streptomycin and erythromycin, whereas those isolated from pig farm workers showed high resistance to tetracycline, ampicillin and erythromycin. The results of the study provide evidence that the use of antibiotics in pigs as well as the increased resistance of intestinal commensal bacteria affects the resistance of intestinal commensal bacteria in the persons working on the farms.
Antibiotic Resistance in Intestinal Commensal Bacteria Isolated from Faecal Samples from Pigs and Pig Farm Workers in Greece
Anastasios Minas,Evanthia Petridou,Eleftheria Bourtzi-Chatzopoulou,Vasilios Krikelis
Research Journal of Biological Sciences , 2008,
Abstract: The increased antibiotic resistance of intestinal commensal bacteria of food-producing animals in the last decade due to the extensive use of antibiotics is a potential risk for human health. In the present study, the prevalence of antibiotic resistance of E. coli, E. faecalis and E. faecium isolated from faecal samples from fattening pigs and pig farm workers who are not in contact with animals (group A) and pig farm workers who are in direct contact with animals (group B) was determined. The resistance of the bacteria was assessed by the determination of Minimum Inhibitory Concentration (MIC) of each antibiotic used in the study by microdilution method. E. coli isolated from fattening pigs showed resistance to at least one antibiotic used in the study at 93.20%, from pig farm workers of group A at 60.19% and of group B at 41.74%. The isolates of E. faecalis from fattening pigs, pig farm workers of group A and pig farm workers of group B were resistant to at least one antibiotic used in the study at 73.78, 68.93 and 52.42%. The resistance of E. faecium isolated from the same groups was determined at 62.13, 52.43 and 44.66%. E. coli and Enterococci isolated from pigs showed high resistance to tetracyclines, sulfamethoxazone, streptomycin and erythromycin, whereas those isolated from pig farm workers showed high resistance to tetracycline, ampicillin and erythromycin. The results of the study provide evidence that the use of antibiotics in pigs as well as the increased resistance of intestinal commensal bacteria affects the resistance of intestinal commensal bacteria in the persons working on the farms.
FORMULATION OF SYNBIOTIC DRINK TO ENHANCE INTESTINAL GUT FLORA  [PDF]
P. L. Sridevi Sivakami
International Journal of Pharmaceutical Sciences and Research , 2011,
Abstract: The transition in diet has lead to an increase in lifestyle disorders and thereby increased dependency on wonder drugs. With increased drug discovery and marketing, there is a compelling trend towards large drug dosage. However, food is judged not only for its nutritive properties but also for its ability to improve the health and well being of consumers, thus leading to the advent of “FUNCTIONAL FOODS”. Probiotic organisms of the gut and prebiotics are two under explored functional foods. Hence the current study was done with the aim of formulating a synbiotic health drink to enhance the intestinal flora. Dietary prebiotic sources like whole wheat, oats, soyabean, samai and artichoke were used in the preparation of the health drink. Whole wheat, samai and soyabean was malted separately, shade dried and powdered. Standard procedure was followed while preparing artichoke powder. All the selected ingredients were blended together along with one gram of lyophilized vacuum dried lactic acid bacillus. Six variations of the drink was prepared and organoleptically evaluated to find the most accepted variation. On sensory evaluation, Variation II was graded to be very good in all aspects like appearance, taste, texture, colour and flavour. Ten grams of the best accepted variation II contained 4.7g of malted soyabean, 2.3g of oats powder, 1.2g each of malted wheat and malted samai and 0.5g of artichoke. The above variation also provided more energy (37.84 Kcal), protein (2.58g), fibre (1.23g) and less fat (0.07g). The nutrient content was analysed in the laboratory for energy, protein, fat, fibre and inulin (3.65g) content. The drink when supplemented was also found to reduce the faecal pathogenic load. Hence it can be concluded that the formulated synbiotic drink was low cost, nutritionally rich and also enhanced the intestinal flora. This drink can sure be considered as a potential nutritional supplement and a ideal alternative to drugs.
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