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

Human gut microbiota plays a key role in the development of obesity. Intestinal flora can regulate energy absorption and nutrition metabolism, increasing the energy harvesting from diet. Alteration of gut flora produces excessive lipopolysaccharide, which, when absorbed into the blood, can induce inflammatory reactions and promote the high-fat diet-associated obesity and metabolic syndrome. Intestinal flora increase visceral fat deposition by lowering the expression of Fiaf in intestinal mucosa. Different immune status also affects the intestinal flora.The gut microbiota is hypothesized to be an environmental factor that contributes to obesity; by interacting with factors such as host and diet, it adjusts the energy metabolism. Antibiotics or probiotics may alter the composition of intestinal microflora and improve the metabolic syndrome, and thus provides new treatment options.
Animals ; Diet, High-Fat ; Gastrointestinal Tract ; microbiology ; Humans ; Inflammation ; etiology ; Mice ; Obesity ; microbiology ; therapy ; Probiotics ; therapeutic use

Colorectal cancer is a common carcinoma of gastrointestinal tract, and its incidence is associated with genetic mutations, environment as well as inflammation. Recent studies have shown that many microorganisms may have played an important role in pathogenesis of colorectal cancer. The common bacteria involved in colorectal cancer are Streptococcus bovis, Helicobacter pylori, Escherichia coli, Bacteroides, and Fusobacterium, etc. The common viruses are Polyomavirus, Epstein Barr virus, Cytomegalovirus and Human papillomavirus, etc. The detailed mechanism of these microorganisms in the pathogenesis of colorectal cancer is unclear, and there are no reports on specific pathogenic microorganisms which cause the disease directly. The direction of future researches will focus on metagenome, metatranscriptome, and metaproteome of microorganisms associated with the incidence of colorectal cancer.
Colorectal Neoplasms ; microbiology ; Helicobacter Infections ; Helicobacter pylori ; Herpesvirus 4, Human ; Humans ; Inflammation ; Papillomaviridae

Periodontitis is an inflammatory disease involving the destruction of both soft and hard tissue in the periodontal region. Although dysbiosis of the local microbial community initiates local inflammation, over-activation of the host immune response directly activates osteoclastic activity and alveolar bone loss. Many studies have reported on the cytokine network involved in periodontitis and its crucial and pleiotropic effect on the recruitment of specific immunocytes, control of pathobionts and induction or suppression of osteoclastic activity. Nonetheless, particularities in the stimulation of pathogens in the oral cavity that lead to the specific and complex periodontal cytokine network are far from clarified. Thus, in this review, we begin with an up-to-date aetiological hypothesis of periodontal disease and summarize the roles of cytokines in the host immune response. In addition, we also summarize the latest cytokine-related therapeutic measures for periodontal disease.
Alveolar Bone Loss ; etiology ; Cytokines ; metabolism ; physiology ; Humans ; Inflammation ; Periodontal Diseases ; Periodontitis ; immunology ; microbiology ; Tumor Necrosis Factor-alpha ; physiology

This study was conducted to investigate the association between Helicobacter pylori (H. pylori) infection and the lipid profile among elderly Koreans. A total of 462 subjects (mean age 66.2 +/- 7.6 yr, 84% males) who underwent health check-up were investigated. Each subject underwent gastroduodenoscopy with gastric mucosal biopsy, and H. pylori infection was determined by histopathological examination using the updated Sydney System score. The presence of H. pylori infection was significantly associated with the elevated serum levels of total cholesterol and low density lipoprotein (LDL) cholesterol (P < 0.05 for each) in univariate analysis. H. pylori infection was not associated with triglyceride and high density lipoprotein (HDL) cholesterol levels (P > 0.05 for each). After controlling confounders, multiple logistic regression analysis showed that the odds ratio of H. pylori infection for high LDL cholesterol level (> 140 mg/dL) was 3.113 (95% confidence interval, 1.364-7.018; P = 0.007). There were no significant associations between the presence of H. pylori infection and elevated total cholesterol levels (> 200 mg/dL) in this model (P = 0.586). The results of this study demonstrate that H. pylori infection is associated with the elevated serum LDL cholesterol levels in elderly Koreans, supporting the hypothesis that H. pylori plays a role in promoting atherosclerosis by modifying lipid metabolism.
Aged ; Aged, 80 and over ; Atherosclerosis/microbiology ; Cholesterol, LDL/*blood ; Endoscopy ; Female ; Gastric Mucosa/anatomy & histology/microbiology ; Gastritis ; Helicobacter Infections/*blood/*epidemiology ; *Helicobacter pylori ; Humans ; Inflammation/microbiology ; Male ; Middle Aged ; Peptic Ulcer ; Republic of Korea/epidemiology

BACKGROUND: Infective spondylodiscitis usually occurs in patients of older age, immunocompromisation, co-morbidity, and individuals suffering from an overall poor general condition unable to undergo reconstructive anterior and posterior surgeries. Therefore, an alternative, less aggressive surgical method is needed for these select cases of infective spondylodiscitis. This retrospective clinical case series reports our novel surgical technique for the treatment of infective spondylodiscitis. METHODS: Between January 2005 and July 2011, among 48 patients who were diagnosed with pyogenic lumbar spondylodiscitis or tuberculosis lumbar spondylodiscitis, 10 patients (7 males and 3 females; 68 years and 48 to 78 years, respectively) underwent transpedicular curettage and drainage. The mean postoperative follow-up period was 29 months (range, 7 to 61 months). The pedicle screws were inserted to the adjacent healthy vertebrae in the usual manner. After insertion of pedicle screws, the drainage pedicle holes were made through pedicles of infected vertebra(e) in order to prevent possible seeding of infective emboli to the healthy vertebra, as the same instruments and utensils are used for both pedicle screws and the drainage holes. A minimum of 15,000 mL of sterilized normal saline was used for continuous irrigation through the pedicular pathways until the drained fluid looked clear. RESULTS: All patients' symptoms and inflammatory markers significantly improved clinically between postoperative 2 weeks and postoperative 3 months, and they were satisfied with their clinical results. Radiologically, all patients reached the spontaneous fusion between infected vertebrae and 3 patients had the screw pulled-out but they were clinically tolerable. CONCLUSIONS: We suggest that our method of transpedicular curettage and drainage is a useful technique in regards to the treatment of infectious spondylodiscitic patients, who could not tolerate conventional combined anterior and posterior surgery due to multiple co-morbidities, multiple level infectious lesions and poor general condition.
Aged ; Bone Screws ; Curettage/*methods ; Discitis/blood/microbiology/*surgery ; Drainage/*methods ; Female ; Humans ; Inflammation/blood ; Lumbar Vertebrae/*surgery ; Male ; Middle Aged ; Retrospective Studies ; Treatment Outcome ; Tuberculosis, Spinal/blood/microbiology/surgery

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

Anti-Bacterial Agents ; therapeutic use ; Antibiotic Prophylaxis ; Dry Socket ; drug therapy ; etiology ; Humans ; Inflammation ; drug therapy ; Mandible ; Molar, Third ; microbiology ; surgery ; Surgical Wound Infection ; drug therapy ; etiology ; Tooth Extraction ; adverse effects ; Tooth, Impacted ; microbiology ; surgery

Despite a higher incidence and less favorable outcome of malignant tumors in obese patients, much less recognized is the link between obesity and cancer. The mechanism of the association of obesity with carcinogenesis remains incompletely understood. Postulated mechanisms include insulin resistance, insulin-like growth factor signaling, chronic inflammation, immunomodulation, hyperglycemia-induced oxidative stress, and changes of intestinal microbiome. Insulin resistance leads to direct mitogenic and antiapoptotic signaling by insulin and the insulin-like growth factor axis. Obesity can be considered to be a state of chronic low-grade inflammation. In obesity, numerous proinflammatory cytokines are released from adipose tissue which may involve in carcinogenesis. Hyperglycemia in susceptible cells results in the overproduction of superoxide and this process is the key to initiating all damaging pathways related to diabetes. This hyperglycemia-induced oxidative stress could be one possible link among obesity, diabetes, and cancer development. The role of obesity-related changes in the intestinal microbiome in gastrointestinal carcinogenesis deserves further attention.
Adipokines/metabolism/physiology ; Gastrointestinal Neoplasms/*etiology/microbiology ; Humans ; Inflammation/etiology ; Insulin/metabolism/physiology ; Leptin/metabolism/physiology ; Obesity/*complications/immunology/metabolism ; Oxidative Stress ; Somatomedins/metabolism/physiology

Staphylococcus aureus (S. aureus) is an important human pathogen which can cause a chronic condition with a high relapse rate despite the aggressive antimicrobial treatment. Recent studies showed that intracellular pattern recognition receptors (including NOD) in response to bacteria or bacterial products play a proinflammatory role by activating nuclear transcription factor-κB (NF-κB). But how NOD2 mediates the proinflammatory response to S. aureus in mast cells (MCs) is unclear. So, in this study, we attempted to examine the role of NOD2 in inflammatory responses of MCs to S. aureus. P815 cells (a mouse mast cell line) were cultured. Real-time PCR was used to detect the NOD2 mRNA expression in P815 cells during S. aureus infection. The siRNA against NOD2 gene was synthesized and transfected into S. aureus-infected P815 cells. By using the methods of ELISA and flow cytometry, the effects of NOD2 gene silencing on cell phagocytosis, cytokine secretion, NF-κB activation and cell apoptosis of the S. aureus-infected P815 cells were examined. It was found that S. aureus infection could increase the expression of NOD2 mRNA in P815 cells. NOD2 gene interference in P815 cells reduced the number of S. aureus engulfed by P815 cells, the level of cytokines and the activation of NF-κB. In addition, S. aureus could induce the apoptosis of P815 cells, but NOD2 gene silencing did not affect the cell apoptosis rate. Our data suggested that NOD2 plays a key role in pathogen recognition, signal transduction, and NF-κB activation in the inflammatory responses of MCs infected by S. aureus.
Animals ; Cell Line ; Cytokines ; immunology ; Inflammation Mediators ; immunology ; Mast Cells ; immunology ; microbiology ; Mice ; NF-kappa B ; immunology ; Nod2 Signaling Adaptor Protein ; immunology ; Staphylococcus aureus ; physiology