Antibodies to various mycoplasmas in patients with coronary heart disease.

BACKGROUND: Clinical and epidemiologic features of coronary heart disease may not be explained solely by established risk factors. The role of infectious pathogens in the development and rupture of atherosclerotic plaques remains elusive but an association between Chlamydia pneumoniae, Mycoplasma pneumoniae and CHD has been reported previously. OBJECTIVES: To determine whether there is an association between mycoplasmal infections and CHD. METHODS: We conducted a prospective cohort analysis of 150 consecutive hospitalized patients with CHD (85 with acute coronary syndrome and 65 admitted for unrelated reasons) and 98 healthy blood donors. Antibody titers for Mycoplasma pneumoniae, M. fermentans, M. hominis and Ureaplasma urealyticum were measured with the agglutination test or specific enzyme-linked immunosorbent assay in all three groups of patients. RESULTS: Analysis of the antibody titers did not reveal any significant difference in the presence of mycoplasmal antibodies between the patients with ACS, patients with known stable CHD hospitalized for non-CHD reasons, and healthy blood donors. CONCLUSIONS: Determination of specific antibodies did not reveal a significant association among different types of mycoplasmal infection and CHD.

Amniotic fluid intercellular adhesion molecule-1 is a marker for Ureaplasma infection in women with preterm labor.

OBJECTIVE: The objective of the study was to determine the amniotic fluid soluble intercellular adhesion molecule-1 concentrations in women with preterm labor in relation to intra-amniotic infection. STUDY DESIGN: Amniotic fluids from 125 women with preterm labor (78 with preterm delivery and 47 with term deliveries) were examined for both soluble intercellular adhesion molecule-1 concentrations and intra-amniotic infection with Ureaplasma species. A chi2 test, or Fisher's exact test, when appropriate, was used for statistical analysis. RESULTS: In the preterm delivery group, 45% (35 of 78) had intra-amniotic infection with Ureaplasma species, compared with 19% (9 of 47) in the term delivery group (P = .004). In women with intra-amniotic infection, 26% (9 of 38) had soluble intercellular adhesion molecule-1 levels above 1290 ng/ml. Only 2.3% (1 of 43) in the preterm delivery group without intra-amniotic infection attained this diagnostic level (P = .004). In contrast, there was no significant difference in soluble intercellular adhesion molecule-1 levels between those with or without intra-amniotic infection in the term delivery group. CONCLUSION: Amniotic fluid soluble intercellular adhesion molecule-1 concentrations exceeding 1290 ng/ml can be used as a marker for intra-amniotic infection with Ureaplasma in patients with preterm labor.

Intercellular adhesion molecule-1 concentration, in utero, decreases after antibiotic treatment.

A parturient suffering from preterm premature rupture of membranes at 29-weeks of gestation was hospitalized and staphylococcus was detected in her amniotic fluid. After treatment with antibiotics she delivered a healthy neonate three weeks later. ICAM-1 levels decreased by 20 fold correlating with elimination of the bacteria and prolongation of the pregnancy.

Ureaplasma urealyticum in the development of postpartum endometritis.

OBJECTIVE: Investigation of the clinical significance of Ureaplasma urealyticum and its biovars in the development of postpartum endometritis. STUDY DESIGN: Cervical swabs were cultured for U. urealyticum in women presenting endometritis. The positive U. urealyticum cultures (>10(5) cfu/ml) (study group) were compared with those from women without endometritis (control group). Anti-Ureaplasma antibodies were measured and U. urealyticum biovars were determined by polymerase chain reaction. RESULTS: There was no difference between the prevalence of U. urealyticum in the cervical swabs of both groups, however, the number of cfu per culture, showed a significant difference between study and control groups. Out of the culture positive endometritis patients 39% (26/67) had >10(5) cfu/ml compared to 17% of control patients (5/30) P=0.03. No significant disparity between both the groups was found in the prevalence of the parvo biovar (77% versus 71.5%, respectively). The difference in anti-Ureaplasma antibodies reached no statistical significance (30% versus 18% in study and control groups, respectively). CONCLUSIONS: The significant difference in U. urealyticum culture cfu between both groups suggests that U. urealyticum may play a role in the etiology of this infection. This involvement is dependent not only on the presence or absence of U. urealyticum in the culture, but on its colonization rate in the cervix (>10(5) cfu/ml).

Mycoplasma fermentans inhibits the activity of cellular DNA topoisomerase I by activation of PARP1 and alters the efficacy of its anti-cancer inhibitor.

To understand the effects of the interaction between Mycoplasma and cells on the host cellular function, it is important to elucidate the influences of infection of cells with Mycoplasma on nuclear enzymes such as DNA Topoisomerase type I (Topo I). Human Topo I participates in DNA transaction processes and is the target of anti-cancer drugs, the camptothecins (CPTs). Here we investigated the mechanism by which infection of human tumor cells with Mycoplasma fermentans affects the activity and expression of cellular Topo I, and the anti-cancer efficacy of CPT. Human cancer cells were infected or treated with live or sonicated M. fermentans and the activity and expression of Topo I was determined. M. fermentans significantly reduced (by 80%) Topo I activity in the infected/treated tumor cells without affecting the level of Topo I protein. We demonstrate that this reduction in enzyme activity resulted from ADP-ribosylation of the Topo I protein by Poly-ADP-ribose polymerase (PARP-1). In addition, pERK was activated as a result of the induction of the MAPK signal transduction pathway by M. fermentans. Since PARP-1 was shown to be activated by pERK, we concluded that M. fermentans modified the cellular Topo I activity by activation of PARP-I via the induction of the MAPK signal transduction pathway. Moreover, the infection of tumor cells with M. fermentans diminished the inhibitory effect of CPT. The results of this study suggest that modification of Topo I activity by M. fermentans may alter cellular gene expression and the response of tumor cells to Topo I inhibitors, influencing the anti-cancer capacity of Topo I antagonists.

Mycoplasma pneumonia Infection: A Possible Trigger for Immune Thrombocytopenia.

Mycoplasma pneumonia (M. pneumonia) is usually not considered among the several pathogens that induce immune thrombocytopenia (ITP). We report a child with a clinical diagnosis of severe ITP that was associated with M. pneumonia pneumonia, and review the few cases described in the English literature. We suggest that thrombocytopenia associated with M. pneumonia infection may constitute a subset of ITP, although unlike ITP it occurs concomitantly with the infection and tends to be more severe than "classic" ITP. We recommend that prompt specific antibiotic and immune modulating treatment should be initiated in appropriate clinical settings.

The inhibitory effect of Mycoplasma fermentans on tumour necrosis factor (TNF)-alpha-induced apoptosis resides in the membrane lipoproteins.

Mycoplasma have been shown to be involved in the alteration of several eukaryotic cell functions, such as cytokine production, gene expression and more. We have previously reported that infection of human myelomonocytic U937 cell line with live Mycoplasma fermentans (M. fermentans) inhibited tumour necrosis factor (TNF-alpha)-induced apoptosis. Mycoplasmal membrane lipoproteins are considered to be the most potent initiators of inflammatory reactions in mycoplasmal infections. The aim of this study was to clarify whether the inhibitory effect on TNFalpha-induced apoptosis is exerted by M. fermentans lipoproteins (LPMf). A significant reduction in TNFalpha-induced apoptosis was demonstrated by stimulation of U937 cells with M. fermentans total proteins, LPMf or MALP-2 (M. fermentans synthetic lipopeptide), but not with M. fermentans hydrophilic protein preparation (AqMf). To investigate the mechanism of M. fermentans antiapoptotic effect, the reduction of mitochondrial transmembrane potential (delta psi m) was measured. M. fermentans total proteins LPMf and MALP-2, but not AqMf, inhibited the reduction of delta psi m. In addition, M. fermentans total proteins LPMf and MALP-2, but not AqMf, downregulated the formation of active caspase-8. NF-kappaB was transactivated in cells treated with M. fermentans lipoproteins, and was essential for host cell survival, but not for the inhibition of TNFalpha-induced apoptosis by LPMf. Our results suggest that the inhibitory effect exerted by M. fermentans on TNFalpha-induced apoptosis in U937 cells is due to the membrane lipoproteins of these bacteria.