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.

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.

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.

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.

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.

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.