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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After allogeneic bone marrow transplantation certain patterns of infectious complications emerge that follow the clinical course, are correlated to the immunobiology of transplantation and are almost predictable in their character and expression. The preparative regimen, designed to generate complete aplasia, will be associated with severe and sometimes life-threatening bacterial infections, predominantly with Gram-negative organisms derived from bowel flora, but also Gram-positive skin saprophytes. In this early aplastic phase, life-threatening viral infections are less common, consisting mainly of herpes simplex and possibly Epstein-Barr stomatitis and BK papovavirus cystitis. Systemic infections with invasive filamentous fungi are rare and are seen only when the induced aplasia is markedly prolonged. Once early marrow recovery has been achieved, systemic infections will generally disappear unless acute graft-vs.-host disease develops. This complication, which will lead to the breakdown of natural barriers such as skin and gastrointestinal epithelium and the marked impairment of all systemic defense mechanisms, can cause polymicrobial infections as well as set the stage for life-threatening viral infections. Such opportunistic viral infections, leading to either interstitial pneumonia or hemorrhagic gastroenteritis, are the major threat in the early recovery phase after engraftment has taken place. Usually caused by cytomegalovirus and rotavirus, respectively, these infections are the primary expression of the severe combined immunodeficiency post transplant, statistically associated with the presence of acute graft-vs.-host disease and amenable to immunologic manipulations. With the recovery of cellular and humoral immune function derived from transplanted donor lymphoid cells, the third phase of infectious complications is reached, covering 3 months to 2 years post grafting.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Infections and immunodeficiency in bone marrow transplantation. 304 57

Twelve patients with hematological malignancies were treated with epirubicin and ten patients were evaluable. One out of our four patients with ALL, who had a previous therapy of anthracycline, achieved a partial remission (PR: 25%). In two patients with AML, remission was not obtained. Of four patients with NHL, one with B-cell lymphoma achieved complete remission (CR) and one with ATLL partial remission (CR + PR: 50%). Stomatitis was observed as a major side effect in three patients with acute leukemia and in one with NHL. In conclusion, our trial seems to show the efficacy of epirubicin in lymphoid malignancies.
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PMID:[Single-agent trial with epirubicin in hematological malignancies]. 347 May 33

A variety of lymphoid cell populations were examined in terms of their ability to replicate vesicular stomatitis virus (VSV), a lytic, RNA-containing virus maturing at the cell surface. The number of cells capable of producing VSV was estimated in terms of infectious centers by the virus plaque assay (VPA), and morphologically by electron microscopy (EM). The lymphoid cells examined in this study included: (a) lymph node cells from delayed hypersensitive guinea pigs stimulated by specific antigen, (b) mouse spleen cells activated by selective bone marrow-derived (B) cell and thymus derived (T) cell mitogens, and (c) cells of human and murine continuous lymphoblastoid or lymphoma lines. In unstimulated cultures of guinea pig lymph node cells there is a background of approximately 1 in 1,000 cells which produces VSV; in purified protein derivative (PPD)-stimulated cultures the number of cells producing virus was 1.6% in the VPA and 1.9% by EM. These cells were large lymphocytes with some morphological features of transformed lymphocytes but were not typical blast cells. A few macrophages were associated with virus in both stimulated and control cultures. These observations indicate that (a) cells responsive to antigens, as detected by a marker virus, were lymphocytes; (b) cells other than lymphocytes (macrophages) were capable of replicating VSV even without antigenic stimulation; and (c) the correlation of results obtained by VPA and morphologic examination was usually quite good. Of the total number of mouse spleen cells stimulated with concanavalin (Con A), a T cell mitogen, 4.5 (EM)-5.7% (VPA) were associated with VSV. These were characteristic transformed lymphocytes, similar to phytohemagglutinin (PHA)-stimulated human lymphocytes. In contrast Escherichia coli lipopolysaccharide (LPS)-treated mouse spleen cultures contained lower numbers of virus plaque-forming cells. The majority of such cells associated with virus displayed extensive rough endoplasmic reticulum. Two cultured murine lymphomas containing lymphocytes with the theta surface marker (L5178Y and EL-4) showed a 15-100-fold higher incidence of virus-producing cells than leukemias (L1210 and C57Bl/6) which did not carry this marker. Similarly, the L2C guinea pig leukemia, a known B cell leukemia, yielded a low percent of virus plaque-forming cells (<2%). However, MOPC-104, a plasma cell tumor presumed to be of B cell origin, was found to be an efficient virus producer. There was a wide variation in the efficiency of VSV replication among human lymphoblastoid lines. One line, Wil-2, produced 80% infectious centers after 24 h of exposure to VSV, and all cells were associated with virus at the EM level. The relationship between the virus-producing cells and different lymphocyte subpopulations as well as the efficiency of the two assays for studying virus-producing lymphocytes is discussed.
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PMID:The production of vesicular stomatitis virus by antigen- or mitogen-stimulated lymphocytes and continuous lymphoblastoid lines. 434 76

We tried to transmit human T-cell leukemia virus type I (HTLV-I) into non-lymphoid cells and found that S+L- CCC cat cells were permissive for HTLV-I. Using these HTLV-positive cat cells, vesicular stomatitis virus (VSV) pseudotypes bearing envelope antigens of Japanese isolates of HTLVs were prepared and their reactivities with human or rabbit serum were examined. Japanese HTLV2M, HTLV10Y, and HTLVMT-2 pseudotypes and American HTLVPL pseudotype were neutralized by sera of Japanese and American patients with adult T-cell leukemia/lymphoma (ATL) and rabbit antisera against HTLV. Each serum showed similar antibody titers against different pseudotypes. Thus, envelope antigens of four HTLVs that reacted with the human and rabbit sera were considered to belong to a single serotype.
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PMID:Pseudotype viruses bearing envelope antigens of Japanese isolates of human T-cell leukemia viruses type I. 615 58

When mouse lymphoid cells derived from untreated C57BL/6 mice were cocultivated in liquid cultures with L-cell monolayers for 3 h, overlaid with soft agar, and then further incubated for 12 h, protected foci of L cells against vesicular stomatitis virus infection were formed. Many strains of mice have been found to have the protected focus-forming cells on the L-cell monolayers. The formation of the protected foci was completely suppressed by addition of cycloheximide into soft agar. When anti-interferon (type I) antiserum was added to soft agar, there was a decrease in focus counts of about 80%. These experimental results indicated that the formation of protected foci by untreated mouse lymphoid cells was mediated for the most part by type I interferon that was produced without addition of special inducer. We have designated these focus-forming cells as natural interferon-producing cells (NIPC). NIPC belong to the glass-adherent fraction, and Thy-1 antigen, immunoglobulin, and Ia antigen could not be detected on the surface of the NIPC. NIPC were detected in congenitally athymic nude mice. These findings suggest that NIPC belong to the Ia-negative macrophages. Mouse lymphoid cells obtained from germfree mice could form the protected foci on L-cell monolayers and could produce interferon without the addition of a special inducer. NIPC are considered to be a cellular background for spontaneous interferon production.
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PMID:Natural interferon-producing cells in mice. 616 18

Natural killer (NK) activity and interferon (IFN) production of spleen and bone-marrow lymphocytes were investigated in 8 to 10-wk-old C3HeB/FeJ/Cne mice, before and after in vitro exposure to the synthetic pentapeptide corresponding to positions 32-36 of the sequence of thymopoietin (TP-5). NK activity was studied against the 51Cr-radiolabelled Moloney virus-induced lymphoid cell line YAC 1, while IFN titres were determined by the inhibition of cytopathology of vesicular stomatitis virus on L929 cells, scored for CPE after 24 h from viral infection. A part of the lymphocytes from the spleen and bone marrow were incubated with different preselected doses (0.1, 1 and 10 micrograms/ml) of TP-5 for 1 h at 37 degrees C, and a part were left unincubated. At the end of the incubation time they were tested, without being washed, for NK activity and IFN production. TP-5 was able to significantly enhance (P less than 0.001 chi 2 test with Yate's correction) bone-marrow NK activity at a dose of 1 microgram/ml, while it was ineffective on spleen cells. A decrease of NK activity, seemingly due to a toxic effect, was observed both in bone-marrow and spleen lymphocytes, after incubation with a dose of 10 micrograms/ml. IFN production was not enhanced after exposure to TP-5. In all, our experiments suggest that TP-5 may enhance bone-marrow NK cells, perhaps by permitting the maturation of their precursors, as already known for T-cell-mediated cytotoxicity. Its effect is independent on IFN production and might be able to induce the rearrangement of certain surface specific receptors.
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PMID:In vitro enhancement of bone marrow natural killer cells after incubation with thymopoietin32-36 (TP-5). 619 87

Susceptibility of Syrian hamsters of the inbred LSH and MHA strains to injection of as few as 10 plaque-forming units of vesicular stomatitis virus (VSV) was shown to occur only after intraperitoneal and intrapleural injection and not after injection of VSV intravenously, intranasally, or in the footpads. Despite the fact that fewer LSH hamsters died when VSV was injected via the latter routes, the histopathology of the VSV-induced disease at early times after infection was identical irrespective of the route of virus administration. Histological examination of tissues at various times after administration of VSV by the various routes revealed that VSV exhibited tropism for lymphoreticular tissue, with the greatest amount of necrosis in the splenic periarteriolar lymphoid sheath. A similar pattern also was observed in VSV-infected tissues from genetically resistant UT1 hamsters. Infectivity titrations of various tissues at different times after intraperitoneal injection of VSV revealed that resistant UT1 hamsters began to clear virus from tissues between 40 and 48 h postinfection, whereas virus titers remained high in susceptible animals. Resistance of UT1 hamsters appeared to require an intact spleen since survival of splenectomized animals was less than that of sham-splenectomized UT1 controls. Sublethal whole-body irradiation was also able to reduce resistance of UT1 hamsters (survival was reduced from 100 to 50%). Bone marrow cells from resistant (UT1 X LSH) F1 females were transferred into lethally irradiated susceptible LSH hamsters, and hematopoietic chimeras were produced. After intraperitoneal injection of 100 plaque-forming units of VSV, all of the female chimeras survived, but only 33% of male chimeras survived. These data indicate that resistance to VSV in Syrian hamsters is mediated, at least partially, by cells of hematopoietic origin.
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PMID:Involvement of cells of hematopoietic origin in genetically determined resistance of Syrian hamsters to vesicular stomatitis virus. 627 20

The most marked production of immune interferon by human peripheral blood leukocytes and splenocytes stimulated with phytohemagglutinin (PHA) and staphylococcal enterotoxin A (SEA) was shown to be achieved when lymphoid cells are propagated under conditions of constant sparing mixing on roller apparatus at a temperature of 37 degrees +/- 0.5 degrees C. The resulting interferon was sensitive to low pH, thermolabile, inactivated by treatment with trypsin, and not neutralised by antisera to human alpha- and beta-interferons. The antiviral properties with regard to vesicular stomatitis and Semliki Forest viruses were practically similar in PHA- and SEA-induced interferon and human alpha- and beta-interferons. The capacity to inhibit colony formation by HeLa cells was 30 times higher in gamma-interferon than the antiproliferative activity of alpha- and beta-interferons.
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PMID:[Human immune interferon: production and action]. 632 69

Nine foals with combined immunodeficiency were given hepatic and thymus cells from 68- to 110-day-old (gestational age) fetuses or peripheral blood lymphocytes from nonrelated horses. Clinical signs and lesions consistent with graft vs host reaction were observed in eight of the foals. Diarrhea was observed in these 8 foals, and ulcerative dermatitis, stomatitis, or glossitis was detected in 6 of the 8 foals. Histopathologic changes consisting of necrosis and lymphocyte infiltration were observed in liver, skin, alimentary tract, and less frequently in lymphoid tissues. Changes in complete blood counts, plasma bilirubin concentration, and serum sorbitol dehydrogenase activity were compared with sequential histopathologic alterations in the liver of two combined immunodeficiency foals given peripheral blood lymphocytes from unrelated donor horses. Elevations of sorbitol dehydrogenase correlated with the onset and increasing severity of hepatic lesions.
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PMID:Graft versus host reactions in foals with combined immunodeficiency. 698 99

This study investigated whether or not the localization of persisting Ag influenced the localization of memory B and/or of Ab-forming cells (AFC). As a model Ag, we used vesicular stomatitis virus, which does not measurably replicate extraneuronally in adult mice after peripheral infection. Our results show that memory B cells and AFC are induced at the site where Ag is present; induced memory B cells then recirculate throughout the lymphoid system independently of Ag localization. In contrast, AFC are induced only at the sites of Ag persistence. These triggered Ab producing cells do not recirculate through the lymphoid tissue but migrate to the bone marrow.
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PMID:Free recirculation of memory B cells versus antigen-dependent differentiation to antibody-forming cells. 793 May 64


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