A complex microbiota colonizes mucosal layers in different regions of the human gut. In the healthy state, the microbial communities provide nutrients and energy to the host via fermentation of non-digestible dietary components in the large intestine. In contrast, they can play roles in inflammation and infection, including gastrointestinal diseases and metabolic syndrome such as obesity. However, because of the complexity of the microbial community, the functional connections between the enteric microbiota and metabolism are less well understood. Nevertheless, major progress has been made in defining dominant bacterial species, community profiles, and systemic characteristics that produce stable microbiota beneficial to health, and in identifying their roles in enteric metabolism. Through studies in both mice and humans, we are recently in a better position to understand what effect the enteric microbiota has on the metabolism by improving energy yield from food and modulating dietary components. Achieving better knowledge of this information may provide insights into new possibilities that reconstitution of enteric microbiota via diet can provide the maintenance of healthy state and therapeutic/preventive strategies against metabolic syndrome such as obesity. This review focuses on enteric microbial composition and metabolism on healthy and diseased states.
Animals ; Bacteria/growth & development/metabolism ; Diet ; Gastrointestinal Diseases/*microbiology/pathology ; Humans ; Inflammation/microbiology/pathology ; Intestines/microbiology ; Metabolic Syndrome X/*microbiology/pathology ; *Microbiota ; Probiotics

OBJECTIVETo estimate the effect of the lymph duct ligation on systemic inflammatory factors and endotoxins during intestinal ischemia-reperfusion (I/R).

METHODSMale SD rats underwent occlusion of superior mesenteric artery for 60 min followed by reperfusion for 120 min plus lymph duct ligation or not. Forty rats were randomly divided into 4 groups: group A (blank); group B (sham); group C (intestinal I/R); group D (intestinal I/R plus lymph duct ligation). Mesenteric lymph nodes were harvested for standard bacteriologic cultures. The endotoxin, D-lactate, diamine oxidase (DAO), and cytokines in serum were detected.

RESULTSThe rates of bacterial translocation to mesenteric lymph nodes were 40% in group C and 20% in group D. No positive lymph node cultures were encountered in any of group A and B. The serum cytokines (except for sICAM-1) , D-lactate, DAO and endotoxin levels were lower in group D than those in group C (P<0.05), but both were higher than those in group A and B (P<0.05).

CONCLUSIONDuring intestinal I/R injury, blockage the lymph flow from gut into bloodstream decreases the levels of cytokines, and significantly attenuates the increase in intestinal permeability.

Animals ; Disease Models, Animal ; Inflammation ; Intestinal Diseases ; metabolism ; microbiology ; pathology ; Intestines ; blood supply ; pathology ; Ligation ; Lymph Nodes ; pathology ; Lymphatic System ; surgery ; Male ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism ; microbiology ; pathology

To investigate the mechanism of long non-coding RNA plasmacytoma variant translocation 1 (PVT1) in gastric cancer caused by (HP) infection. The expression of PVT1 was detected by quantitative real-time polymerase chain reaction in HP-infected normal gastric epithelial cells GES-1. Gastric cancer cell line SGC-7901 was transfected with PVT1 small interfering RNA and co-cultured with HP,and then the inflammatory cytokines such as tumor necrosis factor-α (TNF-α),interleukin (IL) -1β,IL-6 and IL-8 were detected. After PVT1 was knocked down,the effects of PVT1 on the proliferation and migration of gastric cancer cells were examined by cell scratch assay. RNA-pulldown combined with mass spectrometry was used to detect the protein binding to PVT1,and the result of mass spectrometry was verified by RNA-pulldown combined with Western blot. In HP-infected normal gastric epithelial cells GES-1,quantitative real-time polymerase chain reaction showed that PVT1 was significantly up-regulated (=7.160,=0.019). PVT1 was knocked down in gastric cancer cells,and then infected with HP. The expressions of inflammatory factors including TNF-α (=3.899,=0.011),IL-1β (=14.610,=0.000),and IL-8 (=6.557,=0.001) were significantly inhibited. Although PVT1 knockdown had no significant effect on the proliferation ability of gastric cancer cells,it inhibited the migration of cells. PVT1 might interact with RPS8 protein. PVT1 may act as a pro-inflammatory factor and regulate gastric cancer caused by HP infection.
Cell Line, Tumor ; Cell Movement ; Cytokines ; metabolism ; Epithelial Cells ; cytology ; microbiology ; Gene Knockdown Techniques ; Helicobacter Infections ; pathology ; Helicobacter pylori ; Humans ; Inflammation ; RNA, Long Noncoding ; genetics

OBJECTIVETo investigated the anti-inflammatory and antimicrobial effects of anthocyanins extracted from black soybean on the chronic bacterial prostatitis (CBP) rat model.

METHODSThe Sprague-Dawley rats were divided into 4 groups, including control, ciprofloxacin, anthocyanins and anthocyanins with ciprofloxacin groups (n=8 in each group). Then, drip infusion of bacterial suspension (Escherichia coli Z17 O:K:H) into Sprague-Dawley rats was conducted to induce CBP. In 4 weeks, results of prostate tissue, urine culture, and histological analysis on the prostate were analyzed for each group.

RESULTSThe use of ciprofloxacin, anthocyanins, and anthocyanins with ciprofloxacin showed statistically significant decreases in bacterial growth and improvements in the reduction of prostatic inflammation compared with the control group (P<0.05). The anthocyanins with ciprofloxacin group showed a statistically significant decrease in bacterial growth and improvement in prostatic inflammation compared with the ciprofloxacin group (P<0.05).

CONCLUSIONSThese results suggest that anthocyanins may have anti-inflammatory and antimicrobial effects, as well as a synergistic effect with ciprofloxacin. Therefore, we suggest that the combination of anthocyanins and ciprofloxacin may be effective in treating CBP to obtain a higher rate of treatment success.

Acinar Cells ; drug effects ; pathology ; Animals ; Anthocyanins ; isolation & purification ; pharmacology ; therapeutic use ; Anti-Infective Agents ; pharmacology ; therapeutic use ; Anti-Inflammatory Agents ; pharmacology ; therapeutic use ; Chronic Disease ; Disease Models, Animal ; Escherichia coli Infections ; drug therapy ; urine ; Fibrosis ; Inflammation ; pathology ; Male ; Plant Extracts ; pharmacology ; therapeutic use ; Prostate ; drug effects ; microbiology ; pathology ; Prostatitis ; drug therapy ; microbiology ; urine ; Rats, Sprague-Dawley ; Severity of Illness Index ; Soybeans ; chemistry ; Urine ; microbiology

OBJECTIVETo study the role of outer membrane protein T (OmpT) in the pathogenesis of uropathogenic Escherichia.coli.

METHODSIn cultured human bladder epithelial cell line 5637, we examined the adhesion ability of wild-type (CFT073), ompT gene knockout (COTD), and revertant (pST) strains of E.coli to the cells and the extracellular matrix (ECM). The expressions of the adhesion gene iha and virulence gene iroN were detected by real-time PCR. Murine models of urinary tract infection with the 3 strains were established to evaluate the bacterial burden of the bladder and kidney tissue and bacterial counts in blood. We also detected the expressions of interleukin-6 (IL-6) and IL-8 in the bladder and kidney tissues of the mice.

RESULTThe COTD strain showed a significantly lower cell adhesion rate than CFT073 strain [(4.62∓0.39)% vs (8.81∓1.13)%, P<0.05] with also a lower ECM-adhesion rate [(4.95∓0.59)% vs (8.85∓0.79)%, P<0.05]. The mRNA expressions of iha and iroN in CFT073 strain were 2.1 and 3.8 times that of COTD strain. In the mouse model, the mean bacterial load of CFT073 strain in the bladder tissue was 6.36∓0.06, significantly greater than that of COTD (6.01∓0.07) and revertant (6.29∓0.06) strains (P<0.05); the bacterial load of CFT073 strain in the kidney tissue was also significantly higher than that of COTD strain (6.25∓0.05 vs 5.87∓0.06, P<0.05). In mice infected with the wild-type, knockout, and revertant strains, the detection rates of IL-6, which were identical to those of IL-8, in the inflammatory bladder and kidney tissues were 60%, 12.5%, and 50%, respectively.

CONCLUSIONSOmpT may regulate the expression of the adhesion gene iha and the transferrin gene iroN to affect the adhesion of uropathogenic E.coli to host cells.

Animals ; Bacterial Adhesion ; Bacterial Load ; Bacterial Outer Membrane Proteins ; metabolism ; Cell Line, Tumor ; Escherichia coli Infections ; pathology ; Escherichia coli Proteins ; metabolism ; Gene Knockout Techniques ; Humans ; Inflammation ; Interleukin-6 ; metabolism ; Interleukin-8 ; metabolism ; Kidney ; microbiology ; Mice ; Peptide Hydrolases ; metabolism ; Receptors, Cell Surface ; metabolism ; Urinary Bladder ; microbiology ; Urinary Tract Infections ; microbiology ; pathology ; Uropathogenic Escherichia coli ; pathogenicity

Animals ; Anti-Bacterial Agents ; administration & dosage ; Escherichia coli ; Female ; Galactosylceramides ; immunology ; Gastric Mucosa ; pathology ; Gastritis, Atrophic ; pathology ; Helicobacter Infections ; complications ; drug therapy ; Helicobacter pylori ; pathogenicity ; Humans ; Inflammation ; pathology ; Intestines ; microbiology ; Levofloxacin ; Lymphocyte Activation ; Male ; Natural Killer T-Cells ; microbiology ; Ofloxacin ; administration & dosage ; Sphingomonas ; Stomach ; pathology

Inflammation is one of the most prominent characteristic features of chronic liver disease, liver fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Most of HCC cases develop in patients with cirrhosis and cirrhosis develops in patients with chronic liver inflammation. Therefore, there is no doubt that there exist some strong connection among inflammation, fibrosis, and cancer. In fact, chronic unresolved inflammation is associated with persistent hepatic injury and concurrent regeneration, leading to sequential development of fibrosis, cirrhosis, and eventually HCC. This review will discuss the common mechanism of inflammation and fibrosis in chronic liver diseases, and then demonstrate why HCC develops in inflammatory and fibrotic conditions.
Carcinoma, Hepatocellular/*etiology ; Gram-Negative Bacteria/growth & development ; Hepatitis, Chronic/*complications/metabolism/microbiology ; Humans ; Hypoxia ; *Inflammation ; Lipopolysaccharides/metabolism ; Liver/metabolism/pathology ; Liver Cirrhosis/*complications ; Liver Neoplasms/*etiology ; Toll-Like Receptors/metabolism

Neutrophils play an essential role in the innate immune response to infection. Neutrophils migrate from the vasculature into the tissue in response to infection. Recently, a neutrophil cell surface receptor, CD177, was shown to help mediate neutrophil migration across the endothelium through interactions with PECAM1. We examined a publicly available gene array dataset of CD177 expression from human neutrophils following pulmonary endotoxin instillation. Among all 22,214 genes examined, CD177 mRNA was the most upregulated following endotoxin exposure. The high level of CD177 expression is also maintained in airspace neutrophils, suggesting a potential involvement of CD177 in neutrophil infiltration under infectious diseases. To determine the role of CD177 in neutrophils in vivo, we constructed a CD177-genetic knockout mouse model. The mice with homozygous deletion of CD177 have no discernible phenotype and no significant change in immune cells, other than decreased neutrophil counts in peripheral blood. We examined the role of CD177 in neutrophil accumulation using a skin infection model with Staphylococcus aureus. CD177 deletion reduced neutrophil counts in inflammatory skin caused by S. aureus. Mechanistically we found that CD177 deletion in mouse neutrophils has no significant impact in CXCL1/KC- or fMLP-induced migration, but led to significant cell death. Herein we established a novel genetic mouse model to study the role of CD177 and found that CD177 plays an important role in neutrophils.
Animals ; Disease Models, Animal ; GPI-Linked Proteins ; genetics ; Gene Expression Regulation ; Genetic Therapy ; Humans ; Immunity, Innate ; genetics ; Inflammation ; genetics ; microbiology ; pathology ; Isoantigens ; genetics ; Mice ; Mice, Knockout ; Neutrophils ; metabolism ; pathology ; Platelet Endothelial Cell Adhesion Molecule-1 ; metabolism ; Receptors, Cell Surface ; genetics ; Staphylococcus aureus ; pathogenicity ; Transcriptional Activation

Houttuynia cordata polysaccharide (HCP) is extracted from Houttuynia cordata, a key traditional Chinese medicine. The study was to investigate the effects of HCP on intestinal barrier and microbiota in H1N1 virus infected mice. Mice were infected with H1N1 virus and orally administrated HCP at a dosage of 40 mg(kg(d. H1N1 infection caused pulmonary and intestinal injury and gut microbiota imbalance. HCP significantly suppressed the expression of hypoxia inducible factor-1α and decreased mucosubstances in goblet cells, but restored the level of zonula occludens-1 in intestine. HCP also reversed the composition change of intestinal microbiota caused by H1N1 infection, with significantly reduced relative abundances of Vibrio and Bacillus, the pathogenic bacterial genera. Furthermore, HCP rebalanced the gut microbiota and restored the intestinal homeostasis to some degree. The inhibition of inflammation was associated with the reduced level of Toll-like receptors and interleukin-1β in intestine, as well as the increased production of interleukin-10. Oral administration of HCP alleviated lung injury and intestinal dysfunction caused by H1N1 infection. HCP may gain systemic treatment by local acting on intestine and microbiota. This study proved the high-value application of HCP.
Animals ; Cytokines ; metabolism ; Drugs, Chinese Herbal ; chemistry ; pharmacology ; therapeutic use ; Gastrointestinal Microbiome ; drug effects ; Houttuynia ; chemistry ; Hypoxia-Inducible Factor 1, alpha Subunit ; metabolism ; Inflammation ; drug therapy ; pathology ; Influenza A Virus, H1N1 Subtype ; pathogenicity ; Intestinal Mucosa ; drug effects ; metabolism ; microbiology ; pathology ; Lung ; drug effects ; metabolism ; pathology ; Male ; Mice, Inbred BALB C ; Orthomyxoviridae Infections ; drug therapy ; pathology ; physiopathology ; Plant Extracts ; chemistry ; Polysaccharides ; chemistry ; pharmacology ; therapeutic use ; Toll-Like Receptors ; metabolism ; Zonula Occludens-1 Protein ; metabolism

Portal vein thrombosis is an uncommon but an important cause of portal hypertension. The most common etiological factors of portal vein thrombosis are liver cirrhosis and malignancy. Albeit rare, portal vein thrombosis can also occur in the presence of local infection and inflammation such as pancreatitis or cholecystitis. A 52-year-old male was admitted because of general weakness and poor oral intake. He had an operation for colon cancer 18 months ago. However, colonic stent had to be inserted afterwards because stricture developed at anastomosis site. Computed tomography taken at admission revealed portal vein thrombosis and inflammation at colonic stent insertion site. Blood culture was positive for Escherichia coli. After antibiotic therapy, portal vein thrombosis resolved. Herein, we report a case of portal vein thrombosis with sepsis caused by inflammation at colonic stent insertion site which was successfully treated with antibiotics.
Anti-Bacterial Agents/therapeutic use ; Cholecystitis/etiology ; Colonic Neoplasms/pathology/therapy ; Escherichia coli/isolation & purification ; Escherichia coli Infections/drug therapy/etiology ; Humans ; Inflammation/*etiology ; Liver/diagnostic imaging ; Male ; Middle Aged ; Pancreatitis/etiology ; Portal Vein ; Sepsis/*diagnosis/drug therapy/microbiology ; Sigmoidoscopy ; Stents/*adverse effects ; Tomography, X-Ray Computed ; Venous Thrombosis/complications/*diagnosis