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

Inoculation of mice and L and human embryonic lung (HEL) cell cultures with Mycoplasma pneumoniae failed to induce the production of interferon. M. pneumoniae multiplied in these cell cultures without a marked cytopathic effect. M. pneumoniae induced interferon in human peripheral blood leukocytes with maximum titres of 32 units/ml at 48 hours after infection.
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PMID:Induction of interferon in mice and cell cultures by Mycoplasma pneumoniae. 2 67

The replication of human cytomegalovirus (CMV) and herpes simplex virus (HSV) was studied in three human embryo cell lines (CMV-Mj-HEL-I, CMV-Mj-HEL-2, and CMV-Mj-HEL-2,T-I) transformed in vitro by human CMV. Growth studies revealed that these cells were completely resistant to infection by CMV strains ADI69 and Mj and partially resistant to HSV types I and 2. Neither virus DNA nor virus proteins were synthesized in the transformed cells infected with CMV AD169. The HSV production in CMV-transformed human embryo lung (HEL) cells was delayed when compared to the virus production in normal HEL cells and spread of HSV c.p.e. was slower in the transformed cells. The treatment of normal HEL cells with a crude extract of CMV-transformed HEL cells also resulted in inhibition of the spread of c.p.e. of HSV types I and 2. The inhibitory effect was not due to interferon since vesicular stomatitis virus replication was not affected and several experiments showed that it was not due to mycoplasma. The presence of virus inhibitor molecules in CMV-transformed cells absent in normal HEL cells is postulated.
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PMID:Replication of herpesviruses in human cells transformed by cytomegalovirus. 21 Nov 87

Mycoplasma pneumoniae, Acholeplasma laidlawii, M. arthritidis, and M. pulmonis were shown to induce interferon in the lymphocyte fraction of ovine peripheral blood leukocytes, but not in the polymorphonuclear leukocyte fraction. Human peripheral blood lymphocytes produced significant levels of interferon in response to infection with M. pneumoniae and M. synoviae. The antiviral substance induced by the mycoplasmas in human lymphocytes was characterized as interferon by the usual criteria.
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PMID:Induction of interferon in ovine and human lymphocyte cultures by mycoplasmas. 98 8

Three strains of Mycoplasma arthritidis were shown to induce marked hyporeactivity in mice to interferon induction by both Newcastle disease virus and poly(I:C). In contrast, the interferon response of mice to tilorone was only partially suppressed by pretreatment of the animals with mycoplasms. Hyporeactivity to Newcastle disease virus was maximal 1 and 3 days after mycoplasms treatment, but the interferon response was maximal 1 day after injection of the mycoplasmas and was no longer apparent by 5 days. No relationship was found between the ability of the mycoplasms themselves to induce interferon and the degree of hyporeactivity produced. These results suggest that mycoplasmas may alter virus-host relationships in vivo.
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PMID:Mycoplasma-mediated hyporeactivity to various interferon inducers. 120 16

Mycoplasmal infection leads to a variety of effects on host cells both in vivo and in vitro. Among these is the induction of interferon, which has been demonstrated in mycoplasma-infected human and sheep lymphoreticular cell cultures and in mice. Different species and strains of mycoplasma vary in their ability to induce interferon in these experimental models. Several studies have shown that mycoplasmas do not elicit the production of interferon in murine cells in vitro or in non-lymphoreticular cells of other animal species. This may be related to the ability of host cells to take up mycoplasmas or to mycoplasma-associated products, such as mycoplasmal viruses. Initial studies of mixed infections with mycoplasmas and animal viruses in vivo have demonstrated both an inhibition and an enhancement of viral disease, indicating the complex nature of mycoplasma-animal virus interactions.
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PMID:Mycoplasma in biological systems: induction of interferon. 127 Feb 62

Cell cultures must be continuously screened for the presence of mycoplasma because, although these microorganisms sometimes pass unnoticed, they may cause chromosomic alterations and interfere with viral replication, antibody and interferon production etc. The International Organization for Mycoplasmology (IOM) recommends the isolation and identification of mycoplasma with a view to the detection of the origin of the infection and the improvement of the quality of the cultures. In this paper, 37 samples belonging to 27 cell lines contaminated with mycoplasma were assayed by the growth inhibition test. It is known that Mycoplasma orale is the most common human mycoplasma contaminant of cell cultures, the major vehicle of contamination being mouth pippeting, while commercial bovine serum in the main source for Mycoplasma arginini and Acholeplasma laidlawii. M. arginini was found in 18 (48.65%) of the cell samples tested, A. laidlawii in 15 (40.55%), and M. orale in two (5.40%). Two other samples could not be identified by the antisera used (antisera against M. arginini, M. orale, Mycoplasma hyorhinis and A. laidlawii) their characteristics being "fried egg" colonies, digitonine sensitivity, Dienes stained, positive glucose catabolism, negative arginini hydrolysis, and negative tetrazolium reduction. No more than one type of mycoplasma was found in each cell culture.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Identification of mycoplasma by the growth inhibition of samples isolated from cell cultures]. 130 16

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

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

The presence of some viral and inframicrobial antigens in peripheral leukocytes was investigated by the indirect immunofluorescence technique in 120 patients with different forms of rheumatism and 50 clinically healthy controls. Mycoplasma pneumoniae and type 3 para-influenza virus were detected most frequently. The determination of serum interferon titer revealed a rise of this product in rheumatic patients.
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PMID:[The incidence of viral and microbial antigens and the serum interferon titer in certain forms of rheumatism]. 172 80

Mycoplasma fermentans-derived high-molecular-weight material (MDHM) was originally discovered because of its capacity to generate, through the induction of monokine synthesis, cytolytic T lymphocytes in concanavalin A-stimulated thymocyte cultures. This study shows that MDHM-activated macrophages not only released interleukin-6 (IL-6) but also exhibited increased synthesis of cell-associated IL-1 as well as liberation of tumor necrosis factor and prostaglandin. We determined 6-keto prostaglandin F1 alpha since it is the stable metabolite of the bioactive prostacyclin. MDHM appeared to be as potent as lipopolysaccharide in inducing the synthesis of these mediators. Priming with gamma interferon further increased MDHM-mediated IL-6 release. Since monokines can be pyrogenic, we tested the effects of an intravenous injection of MDHM on rectal temperatures and leukocyte counts in rabbits. At 1 h after a bolus injection of MDHM, leukocyte counts dropped to about 35% of the initial values, reflecting a decrease in both lymphocytes and granulocytes. At 4 to 6 h after injection, granulocyte counts began to increase again, whereas lymphocyte counts remained low. No leukocytosis was noted during this time. The lack of leukocytosis can be explained by the failure of MDHM-stimulated macrophages to release IL-1. The property of MDHM to cause IL-6 release from macrophages and the IL-6 growth dependency of the 7TD1 hybridoma cell line were made use of in a coculture assay system to quantitate the activity of MDHM. With this method and macrophages from C3H/HeJ lipopolysaccharide-nonresponder mice, MDHM activity was found to be equally distributed in the mycoplasma growth medium and the sedimented mycoplasmas after sonication.
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PMID:MDHM, a macrophage-stimulatory product of Mycoplasma fermentans, leads to in vitro interleukin-1 (IL-1), IL-6, tumor necrosis factor, and prostaglandin production and is pyrogenic in rabbits. 193 55


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