Microbiota Inflammation Research Articles

#395 Gut dysbiosis in ADPKD patients: a controlled pilot study

Abstract Background and Aims Gut dysbiosis has been associated with chronic kidney disease (CKD) and nephrolithiasis and may thus be a factor explaining variability of outcome in autosomal dominant polycystic kidney disease (ADPKD). However, beside a single pilot study the gut microbiome has not been studied in ADPKD. Due to the implications of microbiota in inflammation and crystal formation, we hypothesized that gut dysbiosis could also negatively affect PKD. For this reason, we aimed to characterize the intestinal microbiome in a controlled pilot study of PKD patients and explore the potential impact of dysbiosis on PKD disease progression. Method This study was designed as an observational, cross-sectional controlled pilot study. 25 ADPKD patients were recruited from the AD(H)PKD patient cohort. 12 healthy control subjects were age- and sex matched. Patients with chronic bowel disease were excluded. Serum parameters including eGFR were analyzed around the timepoint of stool collection. The gut microbiome was analyzed by 16S rRNA gene profiling of stool samples. The sequencing data was processed using the DADA2 pipeline and QIIME version 2. Differentially abundant features were identified using linear discriminant analysis (LDA) effect size (LEfSe) analysis. Bacteria-derived serum uremic toxins (total and free Trimethylaminoxid, Indoxylsulfate, p-Cresyl-Sulfate) were measured using liquid chromatography coupled to tandem mass spectrometry (LC- MS/MS). Microbiome data was then correlated with age, kidney function, and markers of PKD disease progression like Mayo classification and early onset of arterial hypertension or urologic complications (<35 years of age). Results Healthy control subjects revealed a significantly higher abundance Actinobacteria (LEfSe LDA score = 3.9, p = 0.025) including probiotic Bifidobacteriaceae (LEfSe LDA score = 3.9, p = 0.021). ADPKD patients displayed a significantly increased abundance of potentially dysbiotic Enterobacteriaceae (LEfSe LDA score = 3.6, p = 0.009). Those findings were independent of kidney function. Most notably, the abundance of Streptococcaceae were significantly overrepresented in PKD patients with Mayo Classes 1D and 1E compared to 1A-1C (p = 0.011). Additionally, early onset of hypertension (< 35 years of age) was associated with an increased abundance of potentially dysbiotic Proteobacteria and a decreased abundance of potentially probiotic Tannerelleaceae. Furthermore, ADPKD patients revealed increased abundance of Peptococcaceae with increasing age and declining kidney function. Finally, serum uremic toxins were significantly increased in ADPKD patients and highly correlated with eGFR. Serum uremic toxins revealed a tendency of positive correlation with the abundance of Peptococcaceae which did not reach statistical significance. Conclusion This controlled pilot study confirms alterations of specific OTUs in PKD patients showing an increase of Enterobacteriaceae and decrease of probiotic Bifidobacteriaceae upon PKD. This suggests a potential shift towards gut dysbiosis. Most notably, the abundance of specific OTUs were observed to be associated with markers of rapid disease progression like Mayo classification 1D and 1E, as well as early onset of arterial hypertension. This suggests for the first time, that gut dysbiosis could affect PKD disease progression. However, it still remains unknown whether gut dysbiosis is caused by ADPKD itself or is a consequence of secondary circumstances such as antibiotic treatment which is common in ADPKD due to frequent urinary tract or cyst infections. Thus, further investigation in larger cohorts is warranted to elucidate the impact of gut microbiota on ADPKD.

281 Effects of Corynebacterium Glutamicum Cell Mass Supplementation on Modulation of Mucosa-Associated Microbiota to Intestinal Health of Nursery Pigs

Abstract The objectives were to evaluate the effects of Corynebacterium glutamicum cell mass (CGCM) supplementation, replacing blood plasma in diets, on the gene expressions of biomarkers associated with peptidoglycan and their correlation with intestinal health in nursery pigs. Weaned pigs (n = 32) were allotted to 4 dietary treatments based on the randomized complete block design with initial BW as blocks. The diets with supplementation of CGCM (0, 0.7, 1.4, and 2.1%) replacing blood plasma up to 1.5% were fed for 21 d. Pigs were euthanized on d 21 to collect proximal and distal jejunal mucosa to measure intestinal health markers. Gene expression of receptors associated with peptidoglycan (PGN) and intestinal health were evaluated by PCR. Correlations between gene expressions of receptors associated with PGN and intestinal health markers in jejunal mucosa were assessed by Pearson’s analysis. Data were analyzed using the Mixed procedure of SAS 9.4. Increasing CGCM supplementation affected (quadratic) the relative gene expression of peptidoglycan recognition protein (PGLYRP) 1 (P = 0.080, max: 1.85% at 1.1% CGCM), PGLYRP4 (P < 0.05, max: 3.24% at 1.2% CGCM), and interferon-γ (P = 0.088, max: 3.25% at 1.1% CGCM). Increasing CGCM supplementation did not affect the relative gene expression of PGLYRP2A, PGLYRP2B, PGLYRP3, Toll-like receptor (TLR) 2, TLR4, Nucleotide-binding oligomerization domain-containing protein (NOD) 1, NOD2, cluster of differentiation (CD) 14, and nuclear factor-kappa B. In proximal jejunal mucosa, PGLYRP1 was positively correlated with immunoglobulin A (IgA) and interleukin 8 (r = 0.50 and 0.45, respectively; P < 0.05). PGLYRP4 was positively correlated with protein carbonyl and IgA (r = 0.65 and 0.60, respectively; P < 0.05). Interferon-γ was positively correlated with Campylobacter coli (r = 0.61; P < 0.05) and IgA (r = 0.52; P < 0.05). PGLYRP2A was negatively correlated (r = -0.44; P < 0.05) with Pseudomonadaceae. TLR2 was positively correlated with Corynebacteriaceae, Pasteurellaceae, and Propionibacteriaceae (r = 0.55, 0.51, and 0.52, respectively; P < 0.05). NOD1 was positively correlated (r = 0.50; P < 0.05) with Propionibacteriaceae. NOD2 were positively correlated with Pasteurellaceae and Propionibacteriaceae (r = 0.73 and 0.53, respectively; P < 0.05). CD14 was negatively correlated (r = -0.47; P < 0.05) with IgA. Campylobacteraceae was positively correlated with tumor necrosis factor-alpha (r = 0.50; P < 0.05). Pseudomonadaceae was negatively correlated with IgG (r = -0.39; P < 0.05). In conclusion, supplementing 1.1% to 1.2% CGCM, replacing 0.8 to 0.9% blood plasma, increased the relative gene expressions of PGLYRP1, PGLYRP4, and interferon-γ, which were related to the modulation of the mucosa-associated microbiota, immune response, and oxidative stress markers caused by CGCM supplementation. Supplementing 2.1% CGCM showed to have a similar expression of receptors associated with PGN and intestinal health by promoting the growth of less inflammatory microbiota.

The regulatory role of gut microbiota in inflammation in depression and anxiety

Numerous studies have identified the important role of the gut microbiota in maintaining of the CNS normal functioning and in the pathogenesis of mental disorders as one of the systems regulating the bidirectional communication between the gut and the brain. The microbiota has been found to be involved in the modulation of inflammation as well as in the development and function of the immune and nervous systems. It is assumed that in multicellular organisms, the nervous and immune systems have evolved together with the microbiota, being in interaction with it, in order to optimize the body's ability to adapt to a wide range of environmental stresses in order to maintain the constancy of its homeostasis. Normally, microbes live in stable communities, while under conditions of even mild or chronic social stress, significant shifts in the composition of the microbiota occur, which lead to the development of dysbiosis associated with changes in microbiota metabolites, which can lead to the formation of physiology and behavior characteristic of stress and depression. Microbes influence the activation of peripheral immune cells that regulate the response to neuroinflammation, brain damage, autoimmune responses, and neurogenesis. The review provides a brief overview of the normal gut microbiota, describes the factors influencing the state of the microbiota, and also discusses recent discoveries concerning the regulatory effect of the gut microbiota on CNS functions, the immune system, and inflammation in the pathogenesis of depression and anxiety.

A Denture Use Model Associated with Candida spp. in Immunocompetent Male and Female Rats.

Denture stomatitis (DS) is a common infection in denture wearers, especially women. This study evaluated the induction of DS using acrylic devices attached to the palate of rats combined with inoculation of Candida spp. Immunocompetent male and female rats received a carbohydrate-rich diet. Impressions were taken from the rats’ palate to individually fabricate acrylic devices. Mono- and multispecies biofilms of C. albicans, C. glabrata, and C. tropicalis were grown on the devices, which were then cemented on posterior teeth and kept in the rats’ palate for four weeks. Microbial samples from the palate and the device were quantified. Oral microbiome of rats inoculated with C. albicans was analyzed by 16S rRNA gene sequencing. Log10(CFU/mL) were analyzed by mixed or two-way MANOVA (α = 0.05). Candida spp. and acrylic device did not induce palatal inflammation macroscopically nor microscopically. Although there was an increase (p < 0.001) of the total microbiota and female rats demonstrated higher (p = 0.007) recovery of Candida spp. from the palate, the gender differences were not biologically relevant. The microbiome results indicate an increase in inflammatory microbiota and reduction in health-associated micro-organisms. Although Candida spp. and acrylic device did not induce DS in immunocompetent rats, the shift in microbiota may precede manifestation of inflammation.

Simotang Alleviates the Gastrointestinal Side Effects of Chemotherapy by Altering Gut Microbiota.

Simotang oral liquid (SMT) is a traditional Chinese medicine (TCM) consisting of four natural plants and is used to alleviate gastrointestinal side effects after chemotherapy and functional dyspepsia (FD). However, the mechanism by which SMT helps cure these gastrointestinal diseases is still unknown. Here, we discovered that SMT could alleviate gastrointestinal side effects after chemotherapy by altering gut microbiota. C57BL/6J mice were treated with cisplatin (DDP) and SMT, and biological samples were collected. Pathological changes in the small intestine were observed, and the intestinal injury score was assessed. The expression levels of the inflammatory factors IL-1β and IL-6 and the adhesive factors Occludin and ZO-1 in mouse blood or small intestine tissue were also detected. Moreover, the gut microbiota was analyzed by high-throughput sequencing of 16S rRNA amplicons. SMT was found to effectively reduce gastrointestinal mucositis after DDP injection, which lowered inflammation and tightened the intestinal epithelial cells. Gut microbiota analysis showed that the abundance of the anti-inflammatory microbiota was downregulated and that the inflammatory microbiota was upregulated in DDP-treated mice. SMT upregulated anti-inflammatory and anticancer microbiota abundance, while the inflammatory microbiota was downregulated. An antibiotic cocktail (ABX) was also used to delete mice gut microbiota to test the importance of gut microbiota, and we found that SMT could not alleviate gastrointestinal mucositis after DDP injection, showing that gut microbiota might be an important mediator of SMT treatment. Our study provides evidence that SMT might moderate gastrointestinal mucositis after chemotherapy by altering gut microbiota.

An in vitro intestinal model captures immunomodulatory properties of the microbiota in inflammation

ABSTRACT Considerable effort has been put forth to understand mechanisms by which the microbiota modulates and responds to inflammation. Here, we explored whether oxidation metabolites produced by the host during inflammation, sodium nitrate and trimethylamine oxide, impact the composition of a human stool bacterial population in a gut simulator. We then assessed whether an immune-competent in vitro intestinal model responded differently to spent medium from bacteria exposed to these cues compared to spent medium from a control bacterial population. The host-derived oxidation products were found to decrease levels of Bacteroidaceae and overall microbiota metabolic potential, while increasing levels of proinflammatory Enterobacteriaceae and lipopolysaccharide in bacterial cultures, reflecting shifts that occur in vivo in inflammation. Spent microbiota media induced elevated intracellular mucin levels and reduced intestinal monolayer integrity as reflected in transepithelial electrical resistance relative to fresh medium controls. However, multiplexed cytokine analysis revealed markedly different cytokine signatures from intestinal cultures exposed to spent medium with added oxidation products relative to spent control medium, while cytokine signatures of cultures exposed to fresh media were similar regardless of addition of host-derived cues. Further, the presence of immune cells in the intestinal model was required for this differentiation of cytokine signatures. This study indicates that simple in vitro immune-competent intestinal models can capture bacterial-mammalian cross-talk in response to host-derived oxidation products and supports utility of these systems for mechanistic studies of interactions between the gut microbiome and host in inflammation.

Loss of C3aR induces immune infiltration and inflammatory microbiota in a new spontaneous model of colon cancer

Abstract Several lines of evidence suggest that inflammation plays a pivotal role in the development and progression of colorectal cancer (CRC) and can be unleashed by the loss of innate immunosurveillance. The complement system is a well characterized first line of defense against pathogens and a central component of the immune response. Emerging evidence suggests that complement anaphylatoxin C3a produced upon complement activation and acting via its receptor (C3aR) may play a role in intestinal homeostasis. However, to date, it is unknown whether and how the C3a/C3aR axis can affect CRC. By mining publicly available datasets, we found that CpG island methylation of c3ar1 occurs in CRC patients and is associated with significant downregulation of C3aR. By reverse-translating this finding we were able to shift in APCMin/+ mice the tumorigenesis from the small intestine to the colon therefore generating a novel mouse model, which more closely mirrors the CRC in humans. Transcriptomic analysis on colorectal polyps from our newly developed genetic mouse model revealed a significant increase in innate and adaptive immune signatures in absence of C3aR. Furthermore, loss of C3aR significantly impacted the fecal and tumor-associated microbiota and supported the blooming of pro-inflammatory bacterial species as confirmed by experiments of fecal microbiota transplantation. Future studies will elucidate whether loss of C3aR can be exploited as a biomarker for sub-groups of CRC and whether the C3a/C3aR axis may be exploited for the generation of more effective therapeutic interventions.

Keywords Index

HelicobacterVolume 25, Issue S1 e12747 KEYWORD INDEX Keywords Index First published: 12 September 2020 https://doi.org/10.1111/hel.12747Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinked InRedditWechat Volume25, IssueS1Special Issue: The Year in Helicobacter. XXXIIIrd International Workshop on Helicobacter & Microbiota in Inflammation & Cancer, Virtual Conference, 12 September 2020September 2020e12747 RelatedInformation

XXXIIIrd International Workshop on Helicobacter & Microbiota in Inflammation & Cancer, Virtual Conference, 12 September 2020.

HelicobacterVolume 25, Issue S1 e12745 ABSTRACT Abstracts First published: 12 September 2020 https://doi.org/10.1111/hel.12745Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinked InRedditWechat Volume25, IssueS1Special Issue: The Year in Helicobacter. XXXIIIrd International Workshop on Helicobacter & Microbiota in Inflammation & Cancer, Virtual Conference, 12 September 2020September 2020e12745 RelatedInformation

The Crosstalk between Prostate Cancer and Microbiota Inflammation: Nutraceutical Products Are Useful to Balance This Interplay?

The human microbiota shows pivotal roles in urologic health and disease. Emerging studies indicate that gut and urinary microbiomes can impact several urological diseases, both benignant and malignant, acting particularly on prostate inflammation and prostate cancer. Indeed, the microbiota exerts its influence on prostate cancer initiation and/or progression mechanisms through the regulation of chronic inflammation, apoptotic processes, cytokines, and hormonal production in response to different pathogenic noxae. Additionally, therapies’ and drugs’ responses are influenced in their efficacy and tolerability by microbiota composition. Due to this complex potential interconnection between prostate cancer and microbiota, exploration and understanding of the involved relationships is pivotal to evaluate a potential therapeutic application in clinical practice. Several natural compounds, moreover, seem to have relevant effects, directly or mediated by microbiota, on urologic health, posing the human microbiota at the crossroad between prostatic inflammation and prostate cancer development. Here, we aim to analyze the most recent evidence regarding the possible crosstalk between prostate, microbiome, and inflammation.

Abstracts

HelicobacterVolume 24, Issue S1 e12647 ABSTRACTS Abstracts First published: 04 September 2019 https://doi.org/10.1111/hel.12647Citations: 2Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume24, IssueS1Special Issue: The Year in Helicobacter. XXXIInd International Workshop on Helicobacter & Microbiota in Inflammation & Cancer, Innsbruck, Austria, 5–7 September 2019September 2019e12647 RelatedInformation

Author Index

HelicobacterVolume 24, Issue S1 e12648 AUTHOR INDEX Author Index First published: 04 September 2019 https://doi.org/10.1111/hel.12648Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Volume24, IssueS1Special Issue: The Year in Helicobacter. XXXIInd International Workshop on Helicobacter & Microbiota in Inflammation & Cancer, Innsbruck, Austria, 5–7 September 2019September 2019e12648 RelatedInformation

Keyword Index

HelicobacterVolume 24, Issue S1 e12649 KEYWORD INDEX Keyword Index First published: 04 September 2019 https://doi.org/10.1111/hel.12649Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Volume24, IssueS1Special Issue: The Year in Helicobacter. XXXIInd International Workshop on Helicobacter & Microbiota in Inflammation & Cancer, Innsbruck, Austria, 5–7 September 2019September 2019e12649 RelatedInformation

A Proinflammatory Gut Microbiota Increases Systemic Inflammation and Accelerates Atherosclerosis.

Several studies have suggested a role for the gut microbiota in inflammation and atherogenesis. A causal relation relationship between gut microbiota, inflammation, and atherosclerosis has not been explored previously. Here, we investigated whether a proinflammatory microbiota from Caspase1-/- ( Casp1-/-) mice accelerates atherogenesis in Ldlr-/- mice. We treated female Ldlr-/- mice with antibiotics and subsequently transplanted them with fecal microbiota from Casp1-/- mice based on a cohousing approach. Autologous transplantation of fecal microbiota of Ldlr-/- mice served as control. Mice were cohoused for 8 or 13 weeks and fed chow or high-fat cholesterol-rich diet. Fecal samples were collected, and factors related to inflammation, metabolism, intestinal health, and atherosclerotic phenotypes were measured. Unweighted Unifrac distances of 16S rDNA (ribosomal DNA) sequences confirmed the introduction of the Casp1-/- and Ldlr-/- microbiota into Ldlr-/- mice (referred to as Ldlr-/-( Casp1-/-) or Ldlr-/-( Ldlr-/-) mice). Analysis of atherosclerotic lesion size in the aortic root demonstrated a significant 29% increase in plaque size in 13-week high-fat cholesterol-fed Ldlr-/-( Casp1-/-) mice compared with Ldlr-/-( Ldlr-/-) mice. We found increased numbers of circulating monocytes and neutrophils and elevated proinflammatory cytokine levels in plasma in high-fat cholesterol-fed Ldlr-/-( Casp1-/-) compared with Ldlr-/-( Ldlr-/-) mice. Neutrophil accumulation in the aortic root of Ldlr-/-( Casp1-/-) mice was enhanced compared with Ldlr-/-( Ldlr-/-) mice. 16S-rDNA-encoding sequence analysis in feces identified a significant reduction in the short-chain fatty acid-producing taxonomies Akkermansia, Christensenellaceae, Clostridium, and Odoribacter in Ldlr-/-( Casp1-/-) mice. Consistent with these findings, cumulative concentrations of the anti-inflammatory short-chain fatty acids propionate, acetate and butyrate in the cecum were significantly reduced in 13-week high-fat cholesterol-fed Ldlr-/-( Casp1-/-) compared with Ldlr-/-( Ldlr-/-) mice. Introduction of the proinflammatory Casp1-/- microbiota into Ldlr-/- mice enhances systemic inflammation and accelerates atherogenesis.

Abstract PR07: Role of the microbiota in inflammation and lung cancer

Abstract We recently conducted the first comprehensive characterization of the lung cancer microbiome, utilizing 16S rRNA gene sequencing of lung tissue from controls and cancer cases, with validation by metagenomics analysis of RNA-seq unmapped reads from lung cancer samples in The Cancer Genome Atlas. Evidence from 16S rRNA and metagenomics analysis indicated that specific bacteria are associated with the development of lung cancer in humans. However, the functional role of bacteria in the inflammatory microenvironment of the lung and the incidence and progression of lung cancer is unknown. Cigarette smoke, the primary risk factor in lung cancer, reduces epithelial barrier integrity and increases susceptibility to infections. We hypothesized that lung colonization with selected bacterial strains will affect the immune microenvironment and accelerate the rate of tumor development in an autochthonous mouse model of lung cancer. Specifically, we focused on Acidovorax, a taxon we found to be enriched in lung squamous cell carcinoma (SCC) from smokers and with TP53 mutations. KrasLSL-G12D/+ and Trp53LSL-R172H/+ mice (KPC mouse model), conditionally expressing oncogenic Kras and a gain-of-function mutant p53 (a combination of mutations commonly found in human lung cancer), were exposed to Acidovorax temperans via intranasal delivery. Two weeks after exposure to 5 x 106 PFU Ad-Cre (specifically activating the conditional alleles in the lungs), mice were randomly assigned to treatment groups. A biweekly intranasal instillation of 109 CFU Acidovorax temperans (ATCC #49666) was administered in PBS and compared with a sham treatment (PBS alone) for a total of six instillations. One week after the last bacteria instillation (13 weeks after Ad-Cre treatment), mice were subjected to magnetic resonance imaging (MRI). We found a significant increase in tumor volume in animals inoculated with Acidovorax temperans as compared to sham-treated animals (p=0.03), and increased lung weight as a percent of total body weight. To delineate the interactions between the bacteria and the immune system of the host, we co-cultured Acidovorax temperans with human primary macrophages. Our findings show that when Acidovorax temperans is engulfed by M2-like macrophages, the phagocytotic activity of the macrophages is attenuated. In addition, when T cells were co-cultured with M2 macrophages pre-exposed to Acidovorax temperans, their cytotoxicity was inhibited. This inhibition was governed by the CD47-SIRPα “Don’t eat me” signal. These preliminary data indicate that Acidovorax temperans contributes to lung tumorigenesis in the presence of activated Kras and mutant p53. We are conducting additional experiments to investigate the specificity of this observation with respect to Acidovorax temperans and to better understand the role of the microbiota in cancer initiation and progression. This abstract is also being presented as Poster B19. Citation Format: Ana I. Robles, Tomer Cooks, Eleazar Vega-Valle, Marie Vetizou, Uriel Rose, Akihiko Miyanaga, Akriti Trehan, Takahiro Oike, Brid M. Ryan, Shurjo Sen, Leigh Greathouse, Giorgio Trinchieri, Curtis C. Harris. Role of the microbiota in inflammation and lung cancer [abstract]. In: Proceedings of the Fifth AACR-IASLC International Joint Conference: Lung Cancer Translational Science from the Bench to the Clinic; Jan 8-11, 2018; San Diego, CA. Philadelphia (PA): AACR; Clin Cancer Res 2018;24(17_Suppl):Abstract nr PR07.

Keyword Intex

HelicobacterVolume 23, Issue S1 e12527 KEYWORD INDEX keyword Intex First published: 10 September 2018 https://doi.org/10.1111/hel.12527Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Volume23, IssueS1Special Issue: XXX1st International Workshop on Helicobacter & Microbiota in Inflammation & Cancer, 14–15 September 2018, Kaunas, LithuaniaSeptember 2018e12527 RelatedInformation

Abstracts

HelicobacterVolume 23, Issue S1 e12525 ABSTRACTS Abstracts First published: 10 September 2018 https://doi.org/10.1111/hel.12525Citations: 3Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Citing Literature Volume23, IssueS1Special Issue: XXX1st International Workshop on Helicobacter & Microbiota in Inflammation & Cancer, 14–15 September 2018, Kaunas, LithuaniaSeptember 2018e12525 RelatedInformation

Keyword Index

HelicobacterVolume 22, Issue S1 e12420 KEYWORD INDEX Keyword Index First published: 10 September 2017 https://doi.org/10.1111/hel.12420Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Volume22, IssueS1Special Issue: XXXth International Workshop on Helicobacter & Microbiota in Inflammation & Cancer, 7–9 September 2017, Bordeaux, FranceSeptember 2017e12420 RelatedInformation

Author Index

HelicobacterVolume 22, Issue S1 e12419 AUTHOR INDEX Author Index First published: 10 September 2017 https://doi.org/10.1111/hel.12419Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Volume22, IssueS1Special Issue: XXXth International Workshop on Helicobacter & Microbiota in Inflammation & Cancer, 7–9 September 2017, Bordeaux, FranceSeptember 2017e12419 RelatedInformation

Editorial: New Translational Insights on Metabolic Syndrome: Obesity, Hypertension, Diabetes and Beyond.

Editorial: New Translational Insights on Metabolic Syndrome: Obesity, Hypertension, Diabetes and Beyond.