Mycoplasma hyorhinis and Mycoplasma fermentans induce cell apoptosis and changes in gene expression profiles of 32D cells

Abstract

Infection of mycoplasmas has been linked to various human diseases including arthritis, pneumonia, infertility and cancer. While Mycoplasma hyorhinis and Mycoplasma fermentans have been detected in gastric adenocarcinomas, the mechanisms underlyine the pathogenesis are unknown. In this study, cell growth kinetics, Hoechst 33258 staining, DNA ladder assays, Western blotting analysis and cDNA microarray assays were performed to investigate the roles of M. hyorhinis and M. fermentans during infection of mammalian cells. Our data demonstrated that these mycoplasmas inhibid the growth of immortalised cell lines (32D and COS-7) ane tumor cell lines (HeLa and AGS). In addition, the infection of the 32D cell line with M. hyorhinis and M. fermentans induced compression of the nucleus, degradation of the cell genome and dysregulation of the expression of genes related to proliferation, apoptosis, tumorigenesis, signaling pathway and metabolism. Apoptosis related proteins Bcl-2, Bid and p53 were down-regulated, Fas was up-regulated and Bax was dysregulated in mycoplasma-infected 32D cells. Together, our data demonstrated that infection of mycoplasmas inhibitd cele growts through modifi cation of gene expression profi les and post-translation modifi cation of proliferation and apoptosis related proteins.

Mycoplasma hyorhinis induces epithelial-mesenchymal transition in gastric cancer cell MGC803 via TLR4-NF-κB signaling

“…Additionally, we observed decreased confluence of MGC803 cells upon M. hyorhinis infection for 48 h, an indicative of increased cell death or/and decreased proliferation. Previous studies showed that acute infection of M. hyorhinis could initiate apoptosis in distinct cell lines [39,40], while we also found stable infection of M. hyorhinis in AGS and MGC803 cells could promote colony formation [6]. Collectively, results of previous reports and our present study demonstrate pleiotropic impacts of M. hyorhinis on cellular phenotypes.…”

Downregulation of caspase-3 alleviates Mycoplasma pneumoniae-induced apoptosis in alveolar epithelial cells

“…Previous studies demonstrated that the number of cleared apoptotic neutrophils and expression of proinflammatory cytokines are elevated in mice with MPP and causes more severe lung inflammation and higher mortality rates (27). Infection with M. pneumoniae can lead to an imbalance in inflammatory responses that induce the transition from apoptosis to cell death, thereby increasing the severity of lung inflammation (28). The strong association between inflammation and cell survival is reflected by the high IL-6 levels, which suppress cell apoptosis by regulating all hallmarks and multiple signaling pathways involved in inflammation (29).…”

Mycoplasma fermentans infection induces human necrotic neuronal cell death via IFITM3-mediated amyloid-β (1–42) deposition

“…1 a). Although previous studies showed that M. fermentans infection promotes immortalization of Epstein-Barr virus (EBV)-infected human peripheral blood mononuclear cells 17 and induces apoptosis in 32D cells 18 , infected SH-SY5Y cells showed more propidium iodide (PI)-staining and weaker annexin V-staining than uninfected controls (Fig. 1 b), indicating that M. fermentans induces necrotic neuronal cell death, not apoptosis.…”