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Virus Research Sep 2020The first porcine Sapovirus (SaV) Cowden strain was discovered in 1980. To date, eight genogroups (GIII, V-IX) and three genogroups (GIII, GV, and GVI) of porcine SaVs... (Review)
Review
The first porcine Sapovirus (SaV) Cowden strain was discovered in 1980. To date, eight genogroups (GIII, V-IX) and three genogroups (GIII, GV, and GVI) of porcine SaVs have been detected from domestic pigs worldwide and wild boars in Japan, respectively based on the capsid sequences. Although GIII Cowden strain replicated in the villous epithelial cells and caused intestinal lesions in the proximal small intestines (mainly in duodenal and less in jejunum), leading to mild to severe diarrhea, in the orally inoculated neonatal gnotobiotic pigs, the significance of porcine SaVs in different ages of pigs with diarrhea in the field is still undetermined. This is due to two reasons: 1) similar prevalence of porcine SaVs was detected in diarrheic and non-diarrheic pigs; and 2) co-infection of porcine SaVs with other enteric pathogens is common in pigs. Diagnosis of porcine SaV infection is mainly based on the detection of viral nucleic acids using reverse transcription (RT)-PCR and sequencing. Much is unknown about these genetically diverse viruses to understand their role in pig health and to evaluate whether vaccines are needed to prevent SaV infection.
Topics: Animals; Caliciviridae Infections; Diarrhea; Feces; Genetic Variation; Genome, Viral; Phylogeny; RNA, Viral; Sapovirus; Swine; Swine Diseases
PubMed: 32470356
DOI: 10.1016/j.virusres.2020.198025 -
Blood Jun 2023Iron is an essential cellular metal that is important for many physiological functions including erythropoiesis and host defense. It is absorbed from the diet in the...
Iron is an essential cellular metal that is important for many physiological functions including erythropoiesis and host defense. It is absorbed from the diet in the duodenum and loaded onto transferrin (Tf), the main iron transport protein. Inefficient dietary iron uptake promotes many diseases, but mechanisms regulating iron absorption remain poorly understood. By assessing mice that harbor a macrophage-specific deletion of the tuberous sclerosis complex 2 (Tsc2), a negative regulator of mechanistic target of rapamycin complex 1 (mTORC1), we found that these mice possessed various defects in iron metabolism, including defective steady-state erythropoiesis and a reduced saturation of Tf with iron. This iron deficiency phenotype was associated with an iron import block from the duodenal epithelial cells into the circulation. Activation of mTORC1 in villous duodenal CD68+ macrophages induced serine protease expression and promoted local degradation of Tf, whereas the depletion of macrophages in mice increased Tf levels. Inhibition of mTORC1 with everolimus or serine protease activity with nafamostat restored Tf levels and Tf saturation in the Tsc2-deficient mice. Physiologically, Tf levels were regulated in the duodenum during the prandial process and Citrobacter rodentium infection. These data suggest that duodenal macrophages determine iron transfer to the circulation by controlling Tf availability in the lamina propria villi.
Topics: Mice; Animals; Transferrin; Iron, Dietary; Iron; Mechanistic Target of Rapamycin Complex 1; Diet; Duodenum; Receptors, Transferrin
PubMed: 37018657
DOI: 10.1182/blood.2022016632 -
BMC Gastroenterology Feb 2022The purpose of this study was to investigate the diagnosis and treatment experience of traumatic duodenal ruptures in children.
BACKGROUND
The purpose of this study was to investigate the diagnosis and treatment experience of traumatic duodenal ruptures in children.
METHODS
Clinical data were collected from four children suffering from a traumatic duodenal rupture who were admitted to and treated by our hospital from January 2012 to December 2020. The early diagnosis and treatment, surgical plan, postoperative management, complications, and prognosis of each child were analyzed. The key points and difficulties of the diagnosis and treatment for this type of injury are summarized.
RESULTS
One child had an extreme infection caused by drug-resistant bacteria, which resulted in severe complications, including wound infection, dehiscence, and an intestinal fistula. One child developed an anastomotic stenosis after the duodenostomy, which improved following an endoscopic balloon dilatation. The other two children had no relevant complications after their operations. All four patients were cured and discharged from hospital. The average hospital stay was 48.25 ± 26.89 days. The follow-up period was 0.5 to 1 year. No other complications occurred, and all children had a positive prognosis.
CONCLUSIONS
The early identification of a duodenal rupture is essential, and surgical exploration should be carried out proactively. The principles of damage-control surgery should be followed as much as possible during the operation. Multidisciplinary cooperation and management are both important to reduce the occurrence of postoperative complications and improve cure rates.
Topics: Anastomosis, Surgical; Child; Dilatation; Duodenal Diseases; Duodenum; Humans; Postoperative Complications; Retrospective Studies
PubMed: 35151250
DOI: 10.1186/s12876-022-02136-w -
World Journal of Gastroenterology Dec 2021() infection causes changes to the intestinal flora, such as small intestinal bacterial overgrowth, and increases gastric acid secretion-stimulating gastrointestinal...
() infection causes changes to the intestinal flora, such as small intestinal bacterial overgrowth, and increases gastric acid secretion-stimulating gastrointestinal hormones, mainly gastrin, due to a decrease in gastric acid caused by atrophic gastritis. In addition, the cellular components of travel through the intestinal tract, so the bacterial infection affects the immune system. Therefore, the effects of infection are observed not only in the stomach and the proximal duodenum but also in the small and large intestines. In particular, meta-analyses reported that -infected individuals had an increased risk of colorectal adenoma and colorectal cancer. Moreover, a recent study reported that the risk of developing colorectal cancer was increased in subjects carrying vacuolating cytotoxin A antibody. In addition, it has been reported that infection exacerbates the symptoms of Fabry's disease and familial Mediterranean fever attack and is involved in irritable bowel syndrome and small intestinal ulcers. On the other hand, some studies have reported that the frequency of ulcerative colitis, Crohn's disease, and celiac disease is low in -infected individuals. Thus, infection is considered to have various effects on the small and large intestines. However, few studies have reported on these issues, and the details of their effects have not been well elucidated. Therefore, additional studies are needed.
Topics: Crohn Disease; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans
PubMed: 35068852
DOI: 10.3748/wjg.v27.i47.8040 -
Nature May 2019The intestinal immune system has the challenging task of tolerating foreign nutrients and the commensal microbiome, while excluding or eliminating ingested pathogens....
The intestinal immune system has the challenging task of tolerating foreign nutrients and the commensal microbiome, while excluding or eliminating ingested pathogens. Failure of this balance leads to conditions such as inflammatory bowel diseases, food allergies and invasive gastrointestinal infections. Multiple immune mechanisms are therefore in place to maintain tissue integrity, including balanced generation of effector T (T) cells and FOXP3 regulatory T (pT) cells, which mediate resistance to pathogens and regulate excessive immune activation, respectively. The gut-draining lymph nodes (gLNs) are key sites for orchestrating adaptive immunity to luminal perturbations. However, it is unclear how they simultaneously support tolerogenic and inflammatory reactions. Here we show that gLNs are immunologically specific to the functional gut segment that they drain. Stromal and dendritic cell gene signatures and polarization of T cells against the same luminal antigen differ between gLNs, with the proximal small intestine-draining gLNs preferentially giving rise to tolerogenic responses and the distal gLNs to pro-inflammatory T cell responses. This segregation permitted the targeting of distal gLNs for vaccination and the maintenance of duodenal pT cell induction during colonic infection. Conversely, the compartmentalized dichotomy was perturbed by surgical removal of select distal gLNs and duodenal infection, with effects on both lymphoid organ and tissue immune responses. Our findings reveal that the conflict between tolerogenic and inflammatory intestinal responses is in part resolved by discrete gLN drainage, and encourage antigen targeting to specific gut segments for therapeutic immune modulation.
Topics: Animals; CD4 Antigens; Cell Differentiation; Cell Movement; Cell Polarity; Dendritic Cells; Duodenum; Female; Lymph Nodes; Male; Mice; Mice, Inbred C57BL; Mouth; Rats; Rats, Wistar; Stromal Cells; T-Lymphocytes
PubMed: 30988509
DOI: 10.1038/s41586-019-1125-3 -
Journal of Clinical Immunology Feb 2023About 15% of patients with common variable immunodeficiency (CVID) develop a small intestinal enteropathy, which resembles celiac disease with regard to histopathology...
PURPOSE
About 15% of patients with common variable immunodeficiency (CVID) develop a small intestinal enteropathy, which resembles celiac disease with regard to histopathology but evolves from a distinct, poorly defined pathogenesis that has been linked in some cases to chronic norovirus (NV) infection. Interferon-driven inflammation is a prominent feature of CVID enteropathy, but it remains unknown how NV infection may contribute.
METHODS
Duodenal biopsies of CVID patients, stratified according to the presence of villous atrophy (VA), IgA plasma cells (PCs), and chronic NV infection, were investigated by flow cytometry, multi-epitope-ligand cartography, bulk RNA-sequencing, and RT-qPCR of genes of interest.
RESULTS
VA development was connected to the lack of intestinal (IgA) PC, a T helper 1/T helper 17 cell imbalance, and increased recruitment of granzymeCD8 T cells and pro-inflammatory macrophages to the affected site. A mixed interferon type I/III and II signature occurred already in the absence of histopathological changes and increased with the severity of the disease and in the absence of (IgA) PCs. Chronic NV infection exacerbated this signature when compared to stage-matched NV-negative samples.
CONCLUSIONS
Our study suggests that increased IFN signaling and T-cell cytotoxicity are present already in mild and are aggravated in severe stages (VA) of CVID enteropathy. NV infection preempts local high IFN-driven inflammation, usually only seen in VA, at milder disease stages. Thus, revealing the impact of different drivers of the pathological mixed IFN type I/III and II signature may allow for more targeted treatment strategies in CVID enteropathy and supports the goal of viral elimination.
Topics: Humans; Atrophy; Caliciviridae Infections; CD8-Positive T-Lymphocytes; Common Variable Immunodeficiency; Immunoglobulin A; Inflammation; Interferons; Norovirus
PubMed: 36282455
DOI: 10.1007/s10875-022-01379-2 -
World Journal of Gastroenterology Dec 2016() is a gastric human pathogen associated with acute and chronic gastritis, 70% of all gastric ulcers, 85% of all duodenal ulcers, and both forms of stomach cancer,... (Review)
Review
() is a gastric human pathogen associated with acute and chronic gastritis, 70% of all gastric ulcers, 85% of all duodenal ulcers, and both forms of stomach cancer, mucosal-associated lymphoid tissue (MALT) lymphoma and adenocarcinoma. Recently, attention has focused on possible relationship between presence of certain virulence factor and -associated diseases. Some contradictory data between this bacterium and related disorders has been observed since not all the colonized individuals develop to severe disease. The reported diseases plausibility related to specific virulence factors became an interesting story about this organism. Although a number of putative virulence factors have been identified including cytotoxin-associated gene a () and , there are conflicting data about their actual participation as specific risk factor for -related diseases. Duodenal ulcer promoting gene a () is a virulence factor of that is highly associated with duodenal ulcer development and reduced risk of gastric cancer. The prevalence of in strains isolated from western countries is relatively higher than in strains from Asian countries. Current confusing epidemiological reports will continue unless future sophisticated and molecular studies provide data on functional and complete cluster in infected individuals. This paper elucidates available knowledge concerning role of in virulence of after a decade of its discovery.
Topics: Antigens, Bacterial; Asia; Bacterial Proteins; Duodenal Ulcer; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Stomach Neoplasms; Virulence Factors
PubMed: 28028359
DOI: 10.3748/wjg.v22.i46.10118 -
Viruses Aug 2022Norovirus is the most common cause of acute non-bacterial gastroenteritis. Immunocompromised patients can become chronically infected, with or without symptoms. In...
Norovirus is the most common cause of acute non-bacterial gastroenteritis. Immunocompromised patients can become chronically infected, with or without symptoms. In Europe, common variable immunodeficiency (CVID) is one of the most common inborn errors of immunity. A potentially severe complication is CVID-associated enteropathy, a disorder with similar histopathology to celiac disease. Studies suggest that chronic norovirus infection may be a contributor to CVID enteropathy, and that the antiviral drug ribavirin can be effective against norovirus. Here, a patient with CVID-like disease with combined B- and T-cell deficiency, had chronic norovirus infection and enteropathy. The patient was routinely administered subcutaneous and intravenous immunoglobulin replacement therapy (SCIg and IVIg). The patient was also administered ribavirin for ~7.5 months to clear the infection. Stool samples (collected 2013-2016) and archived paraffin embedded duodenal biopsies were screened for norovirus by qPCR, confirming a chronic infection. Norovirus genotyping was done in 25 stool samples. For evolutionary analysis, the capsid (VP1) and polymerase (RdRp) genes were sequenced in 10 and 12 stool samples, respectively, collected before, during, and after ribavirin treatment. Secretor phenotyping was done in saliva, and serum was analyzed for histo-blood group antigen (HBGA) blocking titers. The chronic norovirus strain formed a unique variant subcluster, with GII.4 Den Haag [P4] variant, circulating around 2009, as the most recent common ancestor. This corresponded to the documented debut of symptoms. The patient was a secretor and had HBGA blocking titers associated with protection in immunocompetent individuals. Several unique amino acid substitutions were detected in immunodominant epitopes of VP1. However, HBGA binding sites were conserved. Ribavirin failed in treating the infection and no clear association between ribavirin-levels and quantity of norovirus shedding was observed. In conclusion, long term infection with norovirus in a patient with severe CVID led to the evolution of a unique norovirus strain with amino acid substitutions in immunodominant epitopes, but conservation within HBGA binding pockets. Regularly administered SCIg, IVIg, and ~7.5-month ribavirin treatment failed to clear the infection.
Topics: Blood Group Antigens; Caliciviridae Infections; Common Variable Immunodeficiency; Gastroenteritis; Genotype; Humans; Immunodominant Epitopes; Immunoglobulins, Intravenous; Intestinal Diseases; Norovirus; Ribavirin
PubMed: 36016330
DOI: 10.3390/v14081708 -
American Journal of Infection Control Sep 2016Several clusters of Carbapenem-resistant Enterobacteriaceae (CRE) infections associated with contaminated endoscopes have recently been reported. Interim guidelines for... (Review)
Review
BACKGROUND
Several clusters of Carbapenem-resistant Enterobacteriaceae (CRE) infections associated with contaminated endoscopes have recently been reported. Interim guidelines for mitigating endoscope-associated transmission have been proposed, but there has not been a systematic appraisal of CRE prevention practices.
METHODS
We conducted a systematic review of endoscope-associated CRE infection episodes, abstracting information on outbreak detection, mitigation, outcomes, and corrective steps taken to prevent recurrence.
RESULTS
Seven distinct outbreaks were identified in the published literature, and 5 of these were associated with duodenal endoscopy, with the remaining 2 associated with cystoscopy and ureteroscopy. Several investigators noted difficulties in cleaning protocols surrounding difficult to access components, such as the elevator on duodenoscopes. The published investigations did not report any failures of sterilization. It is unclear if routine reprocessing was ineffective, or difficult to execute properly.
CONCLUSIONS
Meticulous cleaning protocols and increased surveillance are necessary to prevent and detect future outbreaks of CRE and to determine whether more stringent measures, such as sterilization, are needed for duodenoscopes.
Topics: Anti-Bacterial Agents; Carbapenems; Disease Transmission, Infectious; Endoscopy; Enterobacteriaceae; Enterobacteriaceae Infections; Humans; beta-Lactam Resistance
PubMed: 27179395
DOI: 10.1016/j.ajic.2016.03.029 -
BMC Microbiology Jan 2022The bioactivities of commensal duodenal microbiota greatly influence the biofunction of hosts. We investigated the role of Helicobacter pylori infection in...
BACKGROUND
The bioactivities of commensal duodenal microbiota greatly influence the biofunction of hosts. We investigated the role of Helicobacter pylori infection in extra-gastroduodenal diseases by determining the impact of H. pylori infection on the duodenal microbiota. We sequenced 16 S rRNA genes in samples aspirated from the descending duodenum of 47 (male, 20; female, 27) individuals who were screened for gastric cancer. Samples were analysed using 16 S rRNA gene amplicon sequencing, and the LEFSe and Kyoto Encyclopaedia of Genes and Genomes methods were used to determine whether the duodenal microflora and microbial biofunctions were affected using H. pylori infection.
RESULTS
Thirteen and 34 participants tested positive and negative for H. pylori, respectively. We identified 1,404 bacterial operational taxonomic units from 23 phyla and 253 genera. H. pylori infection changed the relative mean abundance of three phyla (Proteobacteria, Actinobacteria, and TM7) and ten genera (Neisseria, Rothia, TM7-3, Leptotrichia, Lachnospiraceae, Megasphaera, F16, Moryella, Filifactor, and Paludibacter). Microbiota features were significantly influenced in H. pylori-positive participants by 12 taxa mostly classified as Gammaproteobacteria. Microbial functional annotation revealed that H. pylori significantly affected 12 microbial metabolic pathways.
CONCLUSIONS
H. pylori disrupted normal bacterial communities in the duodenum and changed the biofunctions of commensal microbiota primarily by upregulating specific metabolic pathways. Such upregulation may be involved in the onset of diseases associated with H. pylori infection.
Topics: Aged; Bacteroidetes; Duodenum; Dysbiosis; Female; Gastric Mucosa; Gastrointestinal Microbiome; Helicobacter Infections; Helicobacter pylori; Humans; Male; Metabolic Networks and Pathways; Microbiota; Middle Aged; Proteobacteria; RNA, Ribosomal, 16S
PubMed: 35033024
DOI: 10.1186/s12866-022-02437-w