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)

Porcine peripheral blood mononuclear cells (PBMC) are induced to produce interferon alpha (IFN alpha) following in vitro exposure to coronavirus TGEV (transmissible gastroenteritis virus)-infected glutaraldehyde-fixed cell monolayers or to TGEV virions. In the present report, we examined the possibility that glycosylation of viral proteins could play a major role in interactions with PBMC leading to the production of IFN alpha. Con A pretreatment of TGEV-infected cell monolayers before fixation with glutaraldehyde and exposure to PBMC caused a dose-dependent inhibition of IFN alpha induction, implying that masking of carbohydrates at the surface of infected cells lowered IFN-alpha-induction. Similarly, inhibition of N-linked glycosylation by tunicamycin during viral infection of cell monolayers altered their ability to induce IFN alpha. In addition, complete cleavage of 'complex type' oligosaccharides by peptide-N-glycohydrolase F lowered the capacity of TGEV virions to induce IFN alpha. Thus, these findings strongly suggest that glycosylation of the viral proteins, and more precisely the presence of complex-type oligosaccharides, is an important requirement for a completely efficient interaction with PBMC leading to the production of IFN-alpha.
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PMID:Glycosylation is required for coronavirus TGEV to induce an efficient production of IFN alpha by blood mononuclear cells. 185 Jan 68

Recombinant DNA-derived bovine interferon alpha 1-1 (BoIFN) inhibited replication of both vesicular stomatitis virus and transmissible gastroenteritis virus in cultures of swine testicular cells. Newborn pigs were orally inoculated with BoIFN and subsequently had interferon in their gastric contents and serum; however, interferon was found only occasionally in intestinal washings. Incubation of BoIFN with gastric contents from a newborn suckling pig did not affect antiviral activity, whereas intestinal (small intestine) contents from the same animal inactivated BoIFN within 1 minute. Beginning at 6 hours of age, newborn, colostrum-deprived pigs were given 1 mg of BoIFN orally every 12 hours. These pigs were not protected against challenge exposure to virulent transmissible gastroenteritis virus at 48 hours of age; disease and mortality were similar for these pigs and for control pigs not given BoIFN prior to challenge exposure. The BoIFN did not impair growth rate of pigs and did not cause obvious disease or lesions.
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PMID:Effect of recombinant DNA-derived bovine alpha-1 interferon on transmissible gastroenteritis virus infection in swine. 371 40

During a natural outbreak of transmissible gastroenteritis (TGE), groups of piglets were treated orally for 4 consecutive days with placebo or 1.0, 10.0 or 20.0 international units (IU) natural human interferon alpha (nHuIFN alpha). Piglets that were 1-12 days of age and given 1.0, 10.0 or 20.0 IU nHuIFN alpha had significantly (P < 0.01) greater survival rates than placebo-treated piglets; survival rates were the greater for the highest level of nHuIFN alpha treatment. In contrast, beneficial effects of nHuIFN alpha were not observed in piglets farrowed during the disease outbreak and given nHuIFN alpha within hours of birth. Oral nHuIFN alpha therapy modulates the natural course of high morbidity and mortality commonly seen with TGE.
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PMID:Oral treatment of transmissible gastroenteritis with natural human interferon alpha: a field study. 767 16

We studied the expression of interferon alpha (IFN alpha)-mRNA in porcine non-adherent peripheral blood mononuclear cells (PBMC) after induction by the coronavirus transmissible gastroenteritis virus (TGEV). We found that protein synthesis inhibition by cycloheximide (CHX) blocked IFN alpha-mRNA expression, except when PBMC were preincubated with a conditioned medium as a potential source of cytokines. These data indicate that IFN alpha-mRNA induction by TGEV requires de novo synthesis of proteins. Moreover, they suggest that IFN alpha-mRNA induction in porcine leukocytes by TGEV involves mechanisms identical to those described for the herpes simplex virus in humans. In addition, experiments performed with a TGEV mutant, dm 49-4, previously characterized for its low ability to induce IFN alpha, showed that addition of a conditioned medium could not normalize its IFN alpha-inducing ability. Therefore, the defect of the dm49-4 mutant may be at the level of the final triggering signal to PBMC.
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PMID:Coronavirus transmissible gastroenteritis virus-mediated induction of IFN alpha-mRNA in porcine leukocytes requires prior synthesis of soluble proteins. 814 54

Porcine blood mononuclear cells (PBMC) were shown to secrete interferon alpha (IFN-alpha) after induction by a coronavirus, the transmissible gastroenteritis virus (TGEV). IFN-alpha producing cells, referred to as natural interferon alpha producing (NIP) cells, were detected by an ELISPOT assay using anti-porcine IFN-alpha monoclonal antibodies. The frequency of NIP cells among blood cells is low, at most 40-110 per 10(5) PBMC and each NIP cell was found to produce several units of IFN. We have shown that NIP cell frequency and IFN yield per cell gradually increased with the age of the donor animals, from the neonatal period to the adult age, with a significant increase around puberty. Our present results also indicate that NIP cells may be influenced by physiological and genetic factors; thus (1) NIP cell frequency and IFN yield per cell were decreased during lactation; (2) Chinese (Meishan) pigs were found to have higher NIP cell frequency and IFN yield per cell than European (Large White) animals.
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PMID:Age-related increase of porcine natural interferon alpha producing cell frequency and of interferon yield per cell. 823 91

Non-infectious UV-inactivated transmissible gastroenteritis virus (TGEV) was previously shown to induce interferon alpha (IFN alpha) secretion following in vitro incubation with blood mononuclear cells. In this study, pig foetuses at different stages of gestation were injected in utero with (a) partially UV-inactivated wild TGEV or (b) fully UV-inactivated wild or dm49-4 mutant TGEV coronavirus. Nucleated cells from foetal liver, bone marrow, spleen and blood were isolated 10 or 20 h after injection and assayed ex vivo for IFN alpha secretion by ELISPOT and ELISA techniques. The administration of TGEV induced IFN alpha-secreting cells in foetal lymphohaematopoietic organs at mid-gestation. In contrast, IFN alpha was not detected in control sham-operated foetuses. A specific point mutation in the amino acid sequence of the viral membrane glycoprotein M of TGEV mutant dm49-4 was associated with lower or absent IFN alpha in utero inducibility by mutant virus as compared with wild virus. Flow cytometry analysis did not show differences in leukocyte surface marker expression between control and TGEV- or between dm49-4 and wild virus-treated foetus cells, with the exception of a reduction in percentages of polymorphonuclear cells in TGEV-treated lymphohaematopoietic tissues, which is probably due to IFN alpha secretion. The present data provided in vivo evidence of IFN alpha secretion at the cell level in foetal lymphohaematopoietic organs. Such IFN alpha-secreting cells in lymphohaematopoietic tissues may be the source of IFN alpha detected during foetal infections.
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PMID:In vivo study of interferon-alpha-secreting cells in pig foetal lymphohaematopoietic organs following in utero TGEV coronavirus injection. 930 May 31

A low frequency leukocyte subpopulation, referred to as natural interferon producing cells (NIPC) is able to produce high amounts of interferon alpha (IFN-alpha) following contact with noninfectious viral structures. In order to examine the possible leukocytic nature and bone marrow origin of NIPC, severe combined immunodeficiency (SCID) mice were reconstituted with porcine leukocyte populations, including bone marrow cells. At different times after reconstitution, enriched CD4 and CD45 positive porcine cells were isolated from various mouse organs and tested for the presence of porcine NIPC by porcine IFN-alpha specific ELISPOT assay, after in vitro stimulation by UV inactivated transmissible gastroenteritis virus (TGEV). Although engraftment of porcine cells in SCID mice was shown by flow cytometry and by the production of pig immunoglobulins, no IFN-alpha secreting cells could be detected. This result suggests that NIPC do not derive from bone marrow precursor cells, or that growth factors needed for in vivo expansion of porcine NIPC were absent in mice.
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PMID:Absence of porcine interferon alpha secreting cells in severe combined immunodeficiency (SCID) mice inoculated with porcine leukocytes. 985 Oct 13

Vibrio parahaemolyticus is the leading cause of gastroenteritis from seafood consumption. We tried to determine how the gene expression levels of intestinal-like epithelial cells (Caco-2 cells) and mouse intestinal loop mucosal cells change upon infection with this bacterium. Since we found the robust production of interferon alpha (IFN-alpha) by the V. parahaemolyticus infection, we also assessed the upregulation of a number of IFN-stimulated genes (ISGs). The expressions of IFN protein were determined by Western blotting, and the gene expressions of Caco-2 cells after V. parahaemolyticus infection were determined by quantitative real-time reverse-transcription polymerase chain reaction. Three ISGs (i.e., IFN-alpha-inducible protein 15, IFN-alpha-inducible protein 6-16, and IFN-induced protein with tetratricopeptide repeats 1) were upregulated by V. parahaemolyticus infection. Infection induced the production of IFN-alpha, but not IFN-beta or IFN-gamma. The upregulation of the 3 ISGs was suppressed by treatment with a neutralizing IFN-alpha antibody. Moreover, the production of infection-induced IFN-alpha was found in the mouse intestinal loop mucosal cells. V. parahaemolyticus infection of Caco-2 cells results in IFN-alpha production and the expression of IFN-regulated genes.
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PMID:Vibrio parahaemolyticus elevates interferon alpha production in intestinal-like epithelial Caco-2 cells. 1802 29

Churg-Strauss syndrome and the hypereosinophilic syndrome share many clinical features, particularly in the early disease stages. Beside blood and tissue eosinophilia, peripheral neuropathies, cutaneous manifestations, eosinophilic alveolitis and gastroenteritis are frequently found. In contrast to the hypereosinophilic syndrome, Churg-Strauss syndrome is defined by the presence of systemic vasculitis. However, frequently symptoms related to eosinophilia are (mis)interpreted as indirect signs of vasculitis. New treatment modalities and diagnostic methods render the early differentiation between Churg-Strauss syndrome and the hypereosinophilic syndrome increasingly clinically important. Patients with hypereosinophilic syndrome should be tested for the presence of the FIP1L1-PDGRFA-mutatition in order to identify patients that could benefit from a treatment with a tyrosine kinase inhibitor such as Imatinib. At present, immunosuppression is still the treatment of first choice for Churg-Strauss syndrome. Novel treatment modalities for both diseases include immunomodulation with interferon alpha and biologics such as antibodies against interleukin 5.
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PMID:[Hypereosinophilic syndrome and Churg-Strauss syndrome: is it clinically relevant to differentiate these syndromes?]. 1821 8