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Query: UMLS:C0026936 (Mycoplasma)
 14,761 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Various species of mycoplasmas were tested for their ability to induce cytokine production in human peripheral blood mononuclear cells (PBMC). Human PBMC were incubated with Mycoplasma pneumoniae, M. hyorhinis, M. arginini, M. salivarium, M. orale, M. gallisepticum or A. laidlawii for 48 hr, and the activities of interleukin-1 beta (IL-1 beta), IL-2, IL-4, IL-6, tumor necrosis factor-alpha (TNF-alpha) and interferon (IFN) in the supernatants were determined by ELISA or bioassay. All mycoplasma species induced IL-1 beta, IL-6 and TNF-alpha, although IL-2 was induced only by M. pneumoniae. IFN was induced by 5 of the 7 species, and the IFN produced was antigenically confirmed to be mainly IFN-alpha. On the other hand, mycoplasma-stimulated cultures did not contain detectable amounts of IFN-beta and IL-4 activities. Furthermore, the cytokines were induced by mycoplasmal contaminating cells in human PBMC as well as by mycoplasma alone. These results suggest that many kinds of cytokines induced by mycoplasma contamination in cell culture affect immunological experiments in vitro.
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PMID:Induction of cytokines in human peripheral blood mononuclear cells by mycoplasmas. 138 Oct 37

This study examined the production of an immunosuppressive factor by the KB and H191 human oral squamous carcinoma cell lines. Conditioned media (CM) from both cell lines markedly inhibited mitogen- and alloantigen-induced proliferation of normal human and rat peripheral blood lymphocytes. By contrast, the proliferation of an exponentially-growing fibroblast cell line remained unchanged by CM. The immunosuppressive factor appeared to act after lymphocyte commitment as indicated by continued blast cell formation, the failure of CM to suppress resting lymphocytes and the fact that CM caused maximum inhibition of lymphocyte proliferation 72 h after the addition of PHA. The addition of exogenous IL-2 did not counteract lymphocyte suppression. Inclusion of indomethacin and isoniazid during cell culture did not significantly alter the degree of suppressive activity. Mycoplasma contamination was absent and CM did not act directly with the thymidine or mitogen. The factor was heat stable at 50 degrees C, acid labile and had a molecular weight in excess of 300 kDa. The results demonstrate that human oral squamous carcinoma cell lines produce an immunosuppressive factor that may have a role in tumour evasion of the host immune response.
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PMID:Production of a suppressor of lymphocyte proliferation by two human oral carcinoma cell lines. 138 28

Recently, the mitogenic effects of the Mycoplasma arthritidis supernatant, MAS, and the induction of interferon-gamma (IFN-gamma) and interleukin-6 (IL-6) by MAS have been described. In the present series of experiments we investigated human peripheral blood mononuclear cells (PBM) and human spleen cells with respect to their production of these and other cytokines. In human spleen cell cultures and PBM, MAS induced the synthesis of interleukin-1 alpha (IL-1 alpha) and IL-1 beta. Both interleukins were secreted faster and in higher amounts by PBM. IL-6 was also induced by MAS in PBM and human spleen cells. The amounts of IL-6 measured by ELISA were higher in PBM, whereas the biological activity of IL-6 was higher in spleen cell cultures. T-cell products such as IL-2, IL-4, and IFN-gamma were also induced by MAS in PBM and spleen cells. The kinetics of IFN-gamma and IL-4 induction were negatively correlated. In PBM we found low levels of IL-4 and high IFN-gamma induction, whereas in spleen cells high titers of IL-4 and low IFN-gamma titers were observed. Collectively, our results indicate that MAS induces different networks of cytokine interactions depending on the organ from which the cells are derived.
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PMID:Induction of cytokines in human peripheral blood and spleen cells by the Mycoplasma arthritidis-derived superantigen. 158 16

The T cell response to microbial T cell mitogens (MTM) such as enterotoxins from Staphylococcus aureus (SE) and the soluble mitogen from Mycoplasma arthritidis, resemble the minor lymphocyte stimulatory locus (Mls) response in several aspects. An important feature of the Mls response is it restriction to CD4+ cells. This study demonstrates that in contrast to Mls, the MTM response includes both CD4+ and CD8+ subsets. Both CD4+ and CD8+ cells expanded in IL-2 after stimulation with SEB showed preferential expression of T cell receptors bearing V beta 8 domains. Mouse and human target cells could be lysed in the presence of MTM both by MTM-stimulated CD8+ lymphocytes and by MHC class I-restricted CTL clones of defined Ag specificity. MTM-induced lysis required the expression of MHC class II, but not class I Ag, on the target cells. Inhibition studies of SEB and Ag-dependent cytolysis by CTL clones underlined the crucial role of CD3 and LFA-1 in both instances, but showed CD8 dependence only for AG-dependent cytolysis. Together these findings suggest important differences between the putative MTM-mediated interaction of TCR with MHC molecules and the classical TCR/MHC interaction involved in MHC-restricted Ag recognition.
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PMID:Activation of MHC class I-restricted CD8+ CTL by microbial T cell mitogens. Dependence upon MHC class II expression of the target cells and V beta usage of the responder T cells. 196 75

Mycoplasma shows a variety of effects on immune system, including the activation of macrophage, the increase in T cell cytotoxicity, and the enhancement of the proliferation and maturation of B cells, etc. As it is well known that many cytokines regulate the immune system, it is interesting to examine whether or not human peripheral blood mononuclear cells (PBMC) produce interleukin (IL) in response to mycoplasmas. In the present study, human PMBC were incubated with 7 species of mycoplasmas for 48 hours, and IL-1 beta, IL-2 and IL-6 activities in the supernatants were determined by ELISA. All the species of mycoplasmas were able to induce IL-1 beta and IL-6, although IL-2 was induced only by M. pneumoniae. These results suggest that the influence of mycoplasma infection on immune system may be partly due to the interleukins induced by mycoplasmas.
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PMID:[Induction of interleukins by mycoplasma in culture of human mononuclear leukocytes]. 215 10

A mitogen derived from supernatants of Mycoplasma arthritidis (MAS) has been shown to induce both T-cell activation and the production of interferon-gamma (IFN-gamma). MAS-induced response required the presence of accessory cells and is under the genetic control associated with the major histocompatibility complex (MHC). We found that recombinant IFN-gamma restored the proliferative response to MAS mitogen in unreactive mice strains, including H-2b and H-2s haplotypes. We postulated that these T-cells fail to respond since they lack part of the I-E molecules on their accessory cells. Our data suggest that interferon-gamma may be able not only to increase the levels of Ia antigens but also to promote the appearance of MHC products that are not usually present on the cell surface. Since Ia antigens have a central role on T-cell activation, we examined the effect of the level of IFN-gamma on MAS-induced T-cell activation. We analyzed the acquisition of responsiveness to IL-2 and IL-2 activity in cells pretreated with IFN-gamma and found that both the steps of T-cell activation were restored to the MAS mitogen in the unreactive mice strains by IFN-gamma.
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PMID:Defective T-cell activation by Mycoplasma arthritidis mitogen is restored by interferon-gamma. 249 88

B lymphocytes, preactivated by lipopolysaccharide (LPS), could be triggered to growth by a strain of Mycoplasma arginini, while the level of immunoglobulin (Ig) secretion, quantitated as the number of plaque-forming cells (PFC), was low. The PFC response could be increased by the addition of conditioned media (CM) from lectin-activated spleen cells or T cell tumour EL-4 to the culture of preactivated B cells. CM did not by itself induce a significant amount of PFC in the cultures of LPS-preactivated B cells. The maturation enhancing activity was distinct from IL-2 and B cell growth factor as judged by gel exclusion chromatography.
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PMID:Enhancement of immunoglobulin secretion by the lymphokine-like activity of a Mycoplasma arginini strain. 348 65

A simple, rapid and sensitive microassay for mycoplasma detection in cell culture is reported. The assay is based on the fact that culture supernatants from contaminated cells inhibit [3H]thymidine incorporation by an IL-2 dependent mouse cytotoxic T cell line (CTLL). The mechanism of inhibition is related to the production by several mycoplasma strains of a pyrimidine-specific nucleoside phosphorylase which can degrade the radiolabelled thymidine used for the measurement of DNA synthesis. These strains were the commonest contaminants in cultures of 24 cell lines from 5 different sources. To establish the sensitivity of the test to detect mycoplasmas we have also used the inhibition assay to monitor the clearance of mycoplasma from 2 contaminated cell lines.
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PMID:A sensitive and quantitative microassay for the detection of mycoplasma contamination: inhibition of IL-2 dependent cell line proliferation. 387 62

Using lectin-free IL-2 as the only initial stimulus, bulk cultures and T-cell clones were established from synovial fluid (SFL) and peripheral blood lymphocytes (PBL) of a patient with rheumatoid arthritis (RA). The cloning efficiency of growing bulk cultures was 3%-4% as evaluated by Poisson statistics and was not enhanced by the addition of autologous synovial fluid or serum. The majority of the cloned T cells expressed the OKT8+ phenotype; several clones were OKT4+ and one clone expressed OKT8+ and OKT4+ antigens. None of the cloned T cells exhibited high NK or lectin-dependent cytotoxicity, although bulk cultures had high NK activity. In primed lymphocyte typing responses, bulk cultures and two T-cell clones established from rheumatoid SFL and PBL showed consistent autoreactivity, which we have never before observed with MLC-derived bulk cultures and T cell clones. One of the autoreactive rheumatoid T-cell clones (B25) was found to provide strong helper activity to autologous B cells in the absence of mitogen. Attempts to reveal reactivity of RA-derived T-cell clones to microbial antigens have so far only been successful with Mycoplasma pneumoniae preparations. Careful analysis of this reactivity revealed, however, that Mycoplasma pneumoniae induces a stimulator cell-dependent mitogenic effect rather than an antigen-specific MHC-restricted T-cell proliferation.
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PMID:Analysis of T-cell cultures and clones from a patient with classic rheumatoid arthritis--evidence for the existence of autoreactive T-cell clones in blood and synovial fluid. 633 24

The objective of this study was to examine the effect of the stimulation of the immune system with Mycoplasma arthritidis superantigen (MAS) on joint inflammation and cartilage destruction. MAS was administered either alone or combined with a model of degenerative arthritis induced by intraarticular injection of collagenase enzyme. Intraperitoneal injection of MAS resulted in activation of peripheral lymphocytes in BALB/c mice, as shown by a proliferative response of splenocytes isolated from MAS-treated animals to IL-2-containing supernatant. Intraperitoneal or intra-articular administration of MAS alone at concentrations maximally activating lymphocytes had no detectable effect on joints. Intra-articular injection of collagenase resulted in some infiltration of inflammatory cells into the joints, hyperplasia and hypertrophy of synovial lining, pannus formation and surface loss of proteoglycans 7 days following the injection. At 21 days, the animals showed almost total loss of cartilage and minimal or no inflammation. Animals receiving MAS in addition to collagenase treatment showed similar changes in the joints. These data have demonstrated that activation of the immune system with MAS in vivo does not increase joint inflammation or cartilage degradation in enzymatically induced arthritis.
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PMID:Effect of Mycoplasma arthritidis superantigen on enzymatically induced arthritis in mice. 788 56


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