Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017160 (gastroenteritis)
 11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human breast milk contains an array of factors with anti-infectious potential, such as immunoglobulins (especially secretory IgA), oligosaccharides and glycoproteins with anti-adhesive capacity, and cytokines. Breast-feeding is associated with protection from the following infections or infection-related conditions: gastroenteritis, upper and lower respiratory tract infection, acute otitis media, urinary tract infection, neonatal septicaemia and necrotizing enterocolitis. Some of the protective effects may derive from an altered mucosal colonization pattern in the breast-fed infant. In other instances breast-fed infants develop less symptoms to the same microbe which causes disease in the bottle-fed infant. An example of an altered colonization pattern is that breast-fed infants have less P-fimbriated, but more type 1-fimbriated E. coli. This may protect against urinary tract infection in the breast-fed infant since P. fimbriae are the major virulence factor for urinary tract infection. An example of changed consequences of the same microbial colonization is that secretory IgA in the breast-milk protects very efficiently from translocation of intestinal bacteria across the gut mucosa by coating intestinal bacteria and blocking their interaction with the epithelium. This mechanism may protect the infant from septicaemia of gut origin and, possibly, necrotizing enterocolitis. Breast-milk is also highly anti-inflammatogenic and contains hormone like factors which counteract diarrhea. Thus, breast-fed infants may be colonized by recognized diarrheal pathogens and still remain healthy. Due to a less virulent intestinal microflora and decreased translocation breast-fed infants will obtain less stimuli for the gut immune system, resulting, in e.g., lower salivary IgA antibody titres.
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PMID:Breast feeding and the intestinal microflora of the infant--implications for protection against infectious diseases. 1106 62

Transmissible gastroenteritis virus (TGEV) infection of piglets results in a very rapid and massive release of IFN-alpha in serum and secretions. The objective of this work was to characterize the IFN-alpha-producing cells (IPC) in tissues of TGEV-infected piglets. Caesarean-derived colostrum-deprived piglets were infected orally with the TGEV virulent Miller strain and IPC were characterized in situ by immunohistochemistry, using a rabbit anti-pig IFN-alpha antiserum. IPC were almost exclusively detected in intestinal tissues and mesenteric lymph nodes (MLN), as early as 6 h post inoculation (p.i.), with a peak at 12-18 h. They disappeared by 24 h. IPC were localized between enterocytes in the small intestine epithelial layer, in the lamina propria, around the Peyer's patches and, at highest frequency, in MLN. Very few IPC were present in the spleen and popliteal lymph nodes of infected piglets. Double immunohistochemical staining for IFN-alpha and leukocyte markers on MLN cryosections showed that IPC were mainly Swine Leukocyte Antigen (SLA) class II positive, and were not stained by an anti-macrophage (SWC3a) MAb. In addition, double staining with anti-TGEV and anti-IFN-alpha MAbs showed that viral antigens were present in MLN, close to IPC. These results show for the first time the presence of IPC in gut mucosa and gut-associated lymphoid tissues in response to an enteropathogenic virus. Moreover, this work shows that IFN-alpha released in serum is likely to originate almost exclusively from gut IPC triggered locally by viral antigens to produce IFN-alpha, since there were very few IPC in spleen or peripheral lymph nodes. MHC class II molecule expression by gut-associated IPC suggests that these cells may be the in vivo mucosal counterparts of the dendritic cells recently shown to produce IFN-alpha after in vitro viral induction.
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PMID:Interferon-alpha-producing cells are localized in gut-associated lymphoid tissues in transmissible gastroenteritis virus (TGEV) infected piglets. 1125 79

Viruses are important causes of diarrhea. In healthy adults, the main clinical manifestation is acute, self-limited gastroenteritis. Advances in molecular diagnostics have shown that epidemics of acute gastroenteritis most frequently are due to caliciviruses spread through contaminated food or through person-to-person contact. Application of similar technology is needed to make a definitive statement about the role of such candidate viruses as rotavirus, astrovirus, and adenovirus as the cause of nonepidemic acute gastroenteritis in adults. Rarely a previously healthy adult gets acute CMV colitis. CMV and EBV mainly cause diarrhea in immunocompromised patients, however. Advances in prophylaxis and treatment have reduced the frequency and severity of these diseases. Acute infantile gastroenteritis is caused by rotavirus, calcivirus, astrovirus, and adenovirus. These viral diseases of the gut are seen by the physician as routine and rare clinical problems.
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PMID:Viral causes of diarrhea. 1158 57

There is considerable interest in the mechanisms that underlie symptom generation in irritable bowel syndrome (IBS) and particularly those mechanisms peripheral to higher centres in the nervous system. While the central nervous system is important in IBS, it is restricted largely to the role of behaviour in stress perception and symptom reporting. The gut and the autonomic nervous system are principal areas of research in identifying mechanisms underlying symptom generation and in the identification of new targets for drug development. While motility changes occur in IBS, they are neither specific nor predictable, and this is one reason why drugs aimed at influencing motility patterns have enjoyed limited success to date. This success has prompted interest in sensory physiology to explain pain and other discomforts expressed by patients with IBS. Patients with IBS exhibit intolerance to rectal distension and other manoeuvres of the gut, while exhibiting normal or raised thresholds for somatic pain. The mechanisms underlying the development of hyperalgesia or allodynia in the gut remain to be determined. In other systems and experimental models, low grade inflammation is a predictable inducer of these states, and recent evidence suggests that a subpopulation of patients with IBS develop chronic symptoms after acute gastroenteritis. This and other inflammatory stimuli may induce a hyperalgesic state and alter motor function in patients with IBS. Substances that mediate these changes are not fully understood, but there is growing recognition of the role of serotonin as a sensitizing agent.
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PMID:Peripheral mechanisms of symptom generation in irritable bowel syndrome. 1169 10

A helper-dependent expression system based on transmissible gastroenteritis coronavirus (TGEV) has been developed using a minigenome of 3.9 kb (M39). Expression of the reporter gene beta-glucuronidase (GUS) (2-8 microg per 10(6) cells) and the porcine respiratory and reproductive syndrome virus (PRRSV) ORF5 (1-2 microg per 10(6) cells) has been shown using a TGEV-derived minigenome. GUS expression levels increased about eightfold with the m.o.i. and were maintained for more than eight passages in cell culture. Nevertheless, instability of the GUS and ORF5 subgenomic mRNAs was observed from passages five and four, respectively. About a quarter of the cells in culture expressing the helper virus also produced the reporter gene as determined by studying GUS mRNA production by in situ hybridization or immunodetection to visualize the protein synthesized. Expression of GUS was detected in the lungs, but not in the gut, of swine immunized with the virus vector. Around a quarter of lung cells showing replication of the helper virus were also positive for the reporter gene. Interestingly, strong humoral immune responses to both GUS and PRRSV ORF5 were induced in swine with this virus vector. The large cloning capacity and the tissue specificity of the TGEV-derived minigenomes suggest that these virus vectors are very promising for vaccine development.
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PMID:In vitro and in vivo expression of foreign genes by transmissible gastroenteritis coronavirus-derived minigenomes. 1184 52

This review focuses on the use and potential of Lactobacillus to prevent infections of the urogenital and intestinal tracts. The presence and dominance of Lactobacillus in the vagina is associated with a reduced risk of bacterial vaginosis and urinary tract infections. The mechanisms appear to involve anti-adhesion factors, by-products such as hydrogen peroxide and bacteriocins lethal to pathogens, and perhaps immune modulation or signaling effects. The instillation of Lactobacillus GR-1 and B-54 or RC-14 strains into the vagina has been shown to reduce the risk of urinary tract infections, and improve the maintenance of a normal flora. Ingestion of these strains into the gut has also been shown to modify the vaginal flora to a more healthy state. In addition, these strains inhibit the growth of intestinal, as well as urogenital pathogens, colonize the gut and protect against infections as shown in mice. Other probiotic strains, such as Lactobacillus GG, have been shown to prevent and treat gastroenteritis caused by rotavirus and bacteria. Given that lactobacilli are not the dominant commensals in a gut which comprises around 10(10) organisms, much work is still needed to define the mechanisms whereby GR-1, RC-14, GG and other strains contribute to health restoration and maintenance. Such critically important studies will require the medical science community to show a willingness to turn away from pharmaceutical remedies as the only solution to health and disease.
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PMID:Use of Lactobacillus to prevent infection by pathogenic bacteria. 1190 42

The potential 'nutritional advantages' of probiotics and prebiotics consist of preventive, and sometimes curative, effects against certain diseases. The evidence supporting such advantages, which requires randomised controlled trials and consistency of results from study to study, is rapidly increasing. This article summarizes the effects against diseases of intestinal origin. There is a high level of evidence for positive effects of some prebiotics to alleviate constipation and treat hepatic encephalopathy. Interesting aspects, but with a lower level of evidence at the present time, include prevention of colon cancer, intestinal infection, and recurrence of inflammatory bowel disease. There is a high level of evidence for positive effects of some probiotics in the alleviation of lactose intolerance, antibiotic-associated intestinal disorders and gastroenteritis. Evidence is rapidly growing regarding the prevention of recurrence of inflammatory bowel diseases. Positive trials have suggested preventive effects against intestinal colonization with specific gut pathogens including Clostridium difficile and Helicobacter pylori.
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PMID:Nutritional advantages of probiotics and prebiotics. 1208 12

Noroviruses are a major cause of epidemic acute nonbacterial gastroenteritis worldwide. Here we report our discovery that recombinant Norwalk virus virus-like particles (rNV VLPs) agglutinate red blood cells (RBCs). Since histo-blood group antigens are expressed on gut mucosa as well as RBCs, we used rNV VLP hemagglutination (HA) as a model system for studying NV attachment to cells in order to help identify a potential NV receptor(s). rNV VLP HA is dependent on low temperature (4 degrees C) and acidic pH. Of the 13 species of RBCs tested, rNV VLPs hemagglutinated only chimpanzee and human RBCs. The rNV VLPs hemagglutinated all human type O (11 of 11), A (9 of 9), and AB (4 of 4) RBCs; however, few human type B RBC samples (4 of 14) were hemagglutinated. HA with periodate- and neuraminidase-treated RBCs indicated that rNV VLP binding was carbohydrate dependent and did not require sialic acid. The rNV VLPs did not hemagglutinate Bombay RBCs (zero of seven) that lack H type 2 antigen, and an anti-H type 2 antibody inhibited rNV VLP HA of human type O RBCs. These data indicated that the H type 2 antigen functions as the rNV VLP HA receptor on human type O RBCs. The rNV VLP HA was also inhibited by rNV VLP-specific monoclonal antibody 8812, an antibody that inhibits VLP binding to Caco-2 cells. Convalescent-phase sera from NV-infected individuals showed increased rNV VLP HA inhibition titers compared to prechallenge sera. In carbohydrate binding assays, the rNV VLPs bound to synthetic Lewis d (Le(d)), Le(b), H type 2, and Le(y) antigens, and these antigens also inhibited rNV VLP HA of human type O RBCs. Overall, our results indicate that carbohydrate antigens in the gut are a previously unrecognized factor in NV pathogenesis.
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PMID:Norwalk virus-like particle hemagglutination by binding to h histo-blood group antigens. 1247 45

Many classes of pathogens excreted in feces are able to initiate waterborne infections. There are bacterial pathogens, including enteric and aquatic bacteria, enteric viruses, and enteric protozoa, which are strongly resistant in the water environment and to most disinfectants. The infection dose of viral and protozoan agents is lower than bacteria, in the range of one to ten infectious units or oocysts. Waterborne outbreaks of bacterial origin (particularly typhoid fever) in the developing countries have declined dramatically from 1900s. Therefore, some early bacterial agents such as Shigella sonnei remains prevalent and new pathogens of fecal origin such as zoonotic C. jejuni and E. coli O157:H7 may contaminate pristine waters through wildlife or domestic animal feces. The common feature of these bacteria is the low inoculum (a few hundred cells) that may trigger disease. The emergence in early 1992 of serotype O139 of V. cholerae with epidemic potential in Southeast Asia suggests that other serotypes than V. cholerae O1 could also getting on epidemic. Some new pathogens include environmental bacteria that are capable of surviving and proliferating in water distribution systems. Other than specific hosts at risk, the general population is refractory to infection with ingested P. aeruginosa. The significance of Aeromonas spp. in drinking water to the occurrence of acute gastroenteritis remains a debatable point and has to be evaluated in further epidemiological studies. Legionella and Mycobacterium avium complex (MAC) are environmental pathogens that have found an ecologic niche in drinking and hot water supplies. Numerous studies have reported Legionnaires' disease caused by L. pneumophila occurring in residential and hospital water supplies. M. avium complex frequently causes disseminated infections in AIDS patients and drinking water has been suggested as a source of infection; in some cases the relationship has been proven. More and more numerous reports show that Helicobacter pylori DNA can be amplified from feces samples of infected patients, which strongly suggests fecal-to-oral transmission. Therefore, it is possible that H. pylori infection is waterbome, but these assumptions need to be substantiated. Giardiasis has become the most common cause of human waterborne disease in the U.S. over the last 30 years. However, as a result of the massive outbreak of waterborne cryptosporidiosis in Milwaukee, Wisconsin, affecting an estimated 403,000 persons, there is increasing interest in the epidemiology and prevention of new infection disease caused by Cryptosporidium spp. as well as monitoring water quality. The transmission of Cryptosporidium and Giardia through treated water supplies that meet water quality standards demonstrates that water treatment technologies have become inadequate, and that a negative coliform no longer guarantees that water is free from all pathogens, especially from protozoan agents. Substantial concern persists that low levels of pathogen occurrence may be responsible for the endemic transmission of enteric disease. In addition to Giardia and Cryptosporidium, some species of genera Cyclospora, Isospora, and of family Microsporidia are emerging as opportunistic pathogens and may have waterborne routes of transmission. More than 15 different groups of viruses, encompassing more than 140 distinct types can be found in the human gut. Some cause illness unrelated with the gut epithelium, such as Hepatitis A virus (HAV) and Hepatitis E virus (HEV). Numerous large outbreaks have been documented in the U.S. between 1950 and 1970, and the incidence rate has strongly declined in developing countries since the 1970s. Hepatitis E is mostly confined to tropical and subtropical areas, but recent reports indicate that it can occur at a low level in Europe. A relatively small group of viruses have been incriminated as causes of acute gastroenteritis in humans and fewer have proven to be true etiologic agents, including rotavirus, calicivirus, astrovirus, and some enteric adenovirus. These enteric viruses have infrequently been identified as the etiologic agents of waterborne disease outbreaks, because of inadequate diagnostic technology, but many outbreaks of unknown etiology currently reported are likely due to viral agents. Actually, Norwalk virus and Norwalk-like viruses are recognized as the major causes of waterborne illnesses world-wide. The global burden of infectious waterborne disease is considerable. Reported numbers highly underestimate the real incidence of waterborne diseases. The most striking concern is that enteric viruses such as caliciviruses and some protozoan agents, such as Cryptosporidium, are the best candidates to reach the highest levels of endemic transmission, because they are ubiquitous in water intended for drinking, being highly resistant to relevant environmental factors, including chemical disinfecting procedures. Other concluding concerns are the enhanced risks for the classic group of debilitated subjects (very young, old, pregnant, and immunocompromised individuals) and the basic requirement of to take specific measures aimed at reducing the risk of waterborne infection diseases in this growing, weaker population.
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PMID:Microbial agents associated with waterborne diseases. 1254 97

Transmissible gastroenteritis coronavirus (TGEV) contains eight overlapping genes that are expressed from a 3'-coterminal nested set of leader-containing mRNAs. To facilitate the genetic manipulation of the viral genome, genes were separated by duplication of transcription regulating sequences (TRSs) and introduction of unique restriction endonuclease sites at the 5' end of each gene using an infectious cDNA clone. The recombinant TGEV (rTGEV) replicated in cell culture with similar efficiency to the wild-type virus and stably maintained the modifications introduced into the genome. In contrast, the rTGEV replication level in the lungs and gut of infected piglets and virulence were significantly reduced. rTGEV in which gene 7 expression was abrogated (rTGEV-delta7) were recovered from cDNA constructs, indicating that TGEV gene 7 was a nonessential gene for virus replication. Interestingly, in vivo infections with rTGEV-delta7 showed an additional reduction in virus replication in the lung and gut, and in virulence, indicating that TGEV gene 7 influences virus pathogenesis.
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PMID:Transmissible gastroenteritis coronavirus gene 7 is not essential but influences in vivo virus replication and virulence. 1270 86


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