Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026936 (Mycoplasma)
 14,761 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In patients infected with Mycoplasma pneumoniae the development of interferon (IFN) was studied in nasopharyngeal secretions and sera. The production of IFN-gamma by lymphocytes was also investigated in response to M. pneumoniae antigen and mumps virus antigen. IFN-alpha was detected in 25 (61.0%) of 41 nasopharyngeal secretion samples and in 25 (59.5%) of 42 serum samples within 6 days after the onset of illness. IFN-alpha was significantly higher in nasopharyngeal secretions than in sera and a significant correlation was observed between the two. In most of the patients lymphocytes produced a larger amount of IFN-gamma in the convalescent stage than in the acute stage, when lymphocytes were stimulated with M. pneumoniae antigen. In some patients, however, lymphocytes did not produce IFN-gamma during the course of illness. Such lymphocytes, negative for IFN-gamma production in response to M. pneumoniae, produced IFN-gamma after the depletion of macrophages, and readdition of macrophages suppressed the production of IFN-gamma by lymphocytes. When lymphocytes were stimulated with heterogeneous antigen (mumps virus), they produced no IFN or a small amount of IFN in the acute stage of M. pneumoniae infection, and IFN production increased in the convalescent stage. Different mechanisms seem to work for homogeneous and heterogeneous antigens in the suppression of IFN production in M. pneumoniae infection.
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PMID:Interferon production during the course of Mycoplasma pneumoniae infection. 137 39

Mycoplasma arthritidis produces a so-far only partially characterized soluble material (MAS) that has a potent mitogenic effect on T lymphocytes of several species. Similar to staphylococcal enterotoxins and a number of related toxins secreted by other species of bacteria, nanogram quantities of these so-called superantigens are sufficient to induce significant amounts of cytokines in the supernatant of lymphocyte cultures. Induction of interleukin-6 (IL-6) by MAS in murine bone marrow-derived macrophages has recently been described. In our study, we examined the differential effects of MAS and Staphylococcus aureus enterotoxin B (SEB) on human blood cells. When compared to MAS, SEB induced a higher proliferative response and, accordingly, a higher release of IFN-gamma. In contrast, large amounts of the macrophage products IL-1, IL-6 and tumor necrosis factor alpha (TNF-alpha) were observed in supernatants of cell cultures stimulated with MAS, whereas only small amounts were induced by SEB. Staphylococci and mycoplasmas are responsible for a number of diseases with various symptoms in man and animals. Our results suggest that SEB and MAS show different qualities in lymphocyte and macrophage stimulation which may be relevant in the pathogenesis of diseases.
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PMID:Induction of cytokines in human whole blood cultures by a mitogen derived from Mycoplasma arthritidis and by staphylococcal enterotoxin B. 149 Jul 30

Several different Mycoplasma species have been shown to act as mitogens for either T or B cells and as stimulators of macrophage tumoricidal activity. In this report, we show that at least five different species of Mycoplasma are capable of inducing class II MHC expression on macrophages. We have observed significant induction of class II MHC surface expression on the myelomonocytic cell line, WEHI-3, as early as 24 h after deliberate infection of cultures, reaching maximal levels by 4 days. This induction was also apparent at the mRNA level as assessed by Northern blot analysis by using A alpha, E alpha, and A beta probes. However, unlike many other previously described MHC-inducing agents, mycoplasmas failed to induce class I MHC expression at either the cell surface or mRNA levels. Kinetic analysis revealed that induction of class II mRNA by mycoplasmas was slower than induction by IFN-gamma requiring 24 h rather than 8 h for significant increases to be noted. Induction by mycoplasmas does not require the presence of live organisms and remains active after heat treatment of 90 degrees C for 30 min. We have also demonstrated that mycoplasma infection of primary bone marrow macrophage cultures leads to the induction of both class I and class II genes and, as in the case of WEHI-3, this induction does not require the presence of live organisms. These data indicate that several Mycoplasma species have the capacity to induce class II MHC expression in WEHI-3 and both class I and class II MHC expression in bone marrow macrophage cultures in the absence of any T cell products.
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PMID:Induction of class II MHC antigen expression in macrophages by Mycoplasma species. 249 74

Recently, a mitogenic effect of the supernatant of cultured mycoplasma arthritidis (MAS) on human and murine lymphocytes has been described. Here, we studied the role of accessory cells (AC) in MAS-induced T cell proliferation in a system of human leukocytes. Nylon-wool purified T cells were non-responsive to MAS with regard to both proliferation and IFN-gamma production. The capacity of T lymphocytes to respond to MAS could be restored when viable AC were added. Treatment of AC with UV light resulted in a cell population which was incapable of reconstituting T cells. Addition of human recombinant interleukin 1 alpha (IL 1 alpha) or IL 1 beta again showed a reconstituting effect. However, only a partial reconstitution of the T cell response could be achieved by addition of recombinant IL 1 alpha or IL 1 beta. The optimal restoration was achieved by adding IL 1 at a concentration of 100 U/ml IL 1 alpha or 100 U/ml IL 1 beta. The results indicate that metabolically active AC were required for MAS-induced T cell proliferation to occur and that IL 1 was able to substitute for the role of AC. Since this restoration was only partial, it remains to be determined whether factors others than IL 1 are required to fully substitute the role of accessory cells.
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PMID:Role of interleukin 1 in mycoplasma mitogen-induced proliferation of human T cells. 249 31

Production of interferon (IFN)-gamma was investigated in human peripheral lymphocytes stimulated with Mycoplasma pneumoniae. Lymphocytes obtained from non-immune individuals produced no IFN. IFN-gamma was produced by T cells obtained from immune individuals, and the helper/inducer T cells produced two- to sixfold higher titer of IFN-gamma than the suppressor/cytotoxic T cells. The addition of macrophages in T cell cultures suppressed the production of IFN-gamma; this differs from the previous result wherein the addition of macrophages enhanced the production of IFN-gamma, when stimulated with mumps virus or measles virus.
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PMID:Suppressive effect of macrophages on interferon-gamma production by human peripheral lymphocytes stimulated with Mycoplasma pneumoniae. 290 15

Regarding of microbiological aspects of arthritis three forms of joint diseases are under investigation: the septic arthritis, the reactive arthritis and the Rheumatoid Arthritis. In 95% of patients with septic arthritis microorganisms as causative agents responsible for the disease are described: Staphylococci, Streptococci, some gram-negative bacteria. By an haematogenic route of infection predominantly patients with immunosuppressive therapy are altered. In newborns and children septic arthritis is to observe more rarely. A reactive arthritis is a postinfectious sterile process in dependence on an infection occurred at an earlier time. As etiologic agents Yersinia, Enterobacteriaceae and Campylobacter have been discovered. 80% of the patients suffering such a reactive arthritis are carrier of the HLA-B27 system. The etiology of the Rheumatoid Arthritis is an open, unanswered problem. Of importance are: immunogenetic conditions, autoimmune phenomena, endocrinologic, dietetic and psychologic factors as well as bacteria and viruses as causative agents: cocci, bacilli, Diphteroids, endoparasitic bacteria (Listeria, L-forms, Mycoplasma, Chlamydiae), viruses (Adeno-, Mumps-, Measles-, ECHO-, Coxsackie-A- and B-, Hepatitis-, Cytomegalo-, Para-influenza-, Retro-, Parvo- and Rubella viruses). In the last years the EBV is of interest covering the question of a distinct virus persistence in tissues and the adequate limiting factors. Perhaps a defect of the hu-IFN-gamma-system might be of immunopathological and clinical significance.
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PMID:[Microbiologic aspects of inflammatory joint diseases]. 367 41

Interferon (IFN) production in mixed cultures of mouse spleen cells and tumor cells was investigated, mainly using mouse myeloid leukemic cells, M1, and spleen cells from syngeneic SL mice. Spleen cells from other mouse strains (C57BL/6, BALB/c nude and C57BL/6 beige) and other tumor cells (L929 and YAC-1) were similarly effective for IFN production, but mouse mammary carcinoma FM3A cells were not. As the IFN-inducing stimulus, mycoplasma contaminating the tumor cells, or endogenous retrovirus in them, may possibly be involved. The type of IFN produced was identified as IFN-gamma as a major component and IFN-alpha and -beta as minor ones, by acid stability tests and neutralization by antisera with defined specificities against alpha, beta, and gamma. Depletion of natural killer cells from spleen cells did not appreciably affect IFN production, but depletion of Thy 1.2 antigen-bearing cells greatly reduced IFN-gamma production, indicating that T cells were the main IFN producers.
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PMID:Interferon production in mixed cultures of mouse spleen cells and tumor cells: IFN-gamma as the main component. 628 16

We have previously shown that a highly tumorigeneic 3-methylcholanthrene transformed clone (MCA-C3H CL 15) of C3H10T1/2 fibroblasts and a normal nontransformed clone (C3H10 1/2 CL 8) from the same parental stock fail to stimulate the generation of syngeneic cytolytic effector cells. In attempting to further dissect and understand the immune response to these cells, we have extended our studies to examine their ability to stimulate the in vitro generation of allogeneic cytolytic effector cells. This model is unique in that studies of immune responses to tumor cells rarely have or utilize appropriate normal cell counterparts. The normal fibroblasts stimulated both the generation of allogeneic cytolytic T lymphocytes (CTL) and the production of immune interferon (IFN-gamma), whereas the tumor fibroblasts did not. The normal fibroblasts were negative for mycoplasma, indicating that these organisms did not account for the observed IFN-gamma induction. When added as third-party cells to cultures containing allogeneic responders and normal fibroblast stimulators, the tumor fibroblasts inhibited the generation of CTL as well as the production of IFN-gamma. The absence of IFN-gamma was not the result of the tumor fibroblasts absorbing or inactivating IFN-gamma, since culturing the tumor cells in IFN-gamma of predetermined activity did not appreciably alter that activity.
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PMID:In vitro inhibition of allogeneic CTL generation and interferon gamma production by the cells of a chemically induced fibrosarcoma. 640 98

Human mitomycin C-treated PBL were mixed with cells of an NK sensitive hybrid cell line (PUTKO-I). A fraction of tumor cells survived this treatment and could be recovered from the cultures. These surviving cells were completely NK-resistant and this property persisted for 2-3 weeks after cultivation in fresh medium. Treatment of a clone (C13) of PUTKO-I with PBL-PUTKO mixed lymphocyte-tumor-cell culture (MLTC) supernatants resulted in a marked reduction in NK sensitivity after 8-12 h of treatment. The kinetics of induction of NK resistance by MLTC supernatants was similar to that of purified IFN-gamma and was faster than for IFN-alpha. The active component in the supernatants was characterized as a mixture of IFN-gamma and IFN-alpha based on neutralization of activity with specific antisera. The role of mycoplasma contamination was investigated and it was found that cell lines free of detectable mycoplasma stimulated production of NK-protective activity by PBL and this activity was neutralized by anti-IFN-gamma serum. Separation of PBL on discontinuous Percoll gradients demonstrated a correlation between the NK activity of cell fractions and their ability to produce IFN in response to tumor cells. Taken together, the selection-dependent variations in NK sensitivity, the kinetics of IFN production and induction of resistance suggest that tumor cells may be able to escape elimination by NK cells due to protection by IFN produced by the effector-cell-containing population.
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PMID:Gamma-interferon (IFN-gamma) produced during effector and target interactions renders target cells less susceptible to NK-cell-mediated lysis. 641 32

Interferon (IFN) stimulates natural killer (NK) cell-mediated lysis of tumor cells. However, it is not clear whether IFN production is essential for NK cells to lyse their target cells in vitro, especially in long-term (greater than 18 hrs) assays. To investigate this, 0.5 X 10(6) normal mouse spleen cells were cocultured in RPMI 1640 medium with Friend erythroleukemia cells (FLD-3) (1 X 10(4] for 24 hours under conditions which cause lysis of FLD-3 cells. Supernatant fluid from such cultures demonstrated antiviral activity (100-200 units) which could be identified as IFN-gamma. Prior filtration of spleen cells over nylon wool, and pretreatment with anti-Thy-1.2 + C' abrogated their ability to generate IFN-gamma without affecting their NK (FLD-3) activity. The IFN-gamma producing cell which could also be detected in spleens of nu/nu BALB/c mice lacked cell surface, Lyt-1, Lyt-2, and NK-1.2 antigens. The stimulus for IFN-gamma induction appeared to be Mycoplasma arginini carried in the FLD-3 tumor cells. Although mycoplasma-free FLD-3 cells failed to induce IFN in vitro, they retained their susceptibility to NK cell-mediated lysis. We conclude that IFN induction is not essential for NK(FLD-3) cell-mediated lysis; indeed IFN detected in NK cell assays may be produced in response to mycoplasma infection of the tumor cells. The Thy-1.2 positive cells stimulated by mycoplasma to produce IFN-gamma lack several characteristics of T-cells or NK cells.
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PMID:Lack of correlation between mycoplasma induced IFN-gamma production in vitro and natural killer cell activity against FLD-3 cells. 642 Mar 33


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