A preliminary study on the potential of Mycoplasma pneumoniae to induce dyskaryotic change in respiratory epithelium in adult community-acquired pneumonia

An, Shuchang; Yang, Donghong; Luo, Chaofeng; Chen, Xin; Liu, Guotian; Weng, Yan; Liu, Jingzhe; Shang, Ying; Wang, Ruiqin; Gao, Zhancheng

doi:10.4103/1735-1995.192497

Cited by 1 publication

(1 citation statement)

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“…Accumulating evidence suggests an association between various species of mycoplasma and human cancers (Huang, Li, Wu, Meng, & Shou, ; Rogers, ). Indeed, dyskaryotic change has been observed in respiratory epithelial cells obtained from patients with M. pneumoniae pneumonia (An et al, ). Therefore, it is possible that the ability of M. pneumoniae to regulate PAR synthesis may contribute to oncogenesis by the bacterium.…”

Section: Discussionmentioning

confidence: 99%

Mycoplasma pneumoniaeprotects infected epithelial cells from hydrogen peroxide‐induced cell detachment

Yamamoto

Kida

Kuwano

2019

Cellular Microbiology

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Epithelial cell shedding is a defence mechanism against infectious microbes that use these cells as an infection foothold and that eliminate microbes from infection foci by removing infected cells. Mycoplasma pneumoniae, a causative agent of respiratory infections, is known to adhere to and colonise the surface of ciliated airway epithelial cells; it produces a large amount of hydrogen peroxide, indicating its capability of regulating hydrogen peroxide-induced infected cell detachment. In this study, we found that M. pneumoniae reduces exogenous hydrogen peroxide-induced detachment of the infected cells from culture plates. This cell detachment occurred dependently of DNA damage-initiated, poly (ADP-ribose) polymerase 1 (PARP1)-mediated cell death, or parthanatos. In cells infected with M. pneumoniae, exogenous hydrogen peroxide failed to induce DNA damage-initiated poly (ADP-ribose) (PAR) synthesis and concomitant increased cytoplasmic membrane rupture, both of which are biochemical hallmarks of parthanatos. The impairment of PAR synthesis was attributed to a reduction in the amount of cytosolic nicotinamide adenine dinucleotide (NAD), a substrate of PARP1, caused by M. pneumoniae. On the other hand, nonadherent mutant strains of M. pneumoniae showed a lower ability to reduce cell detachment than wild-type strains, but the extent to which NAD was decreased in infected cells was comparable to that seen in the wild-type strain. We found that NAD depletion could induce PARP1-independent cell detachment pathways following stimulation with hydrogen peroxide and that M. pneumoniae could also regulate PARP1-independent cell detachment in a cytoadhesion-dependent manner. These results suggest that M.pneumoniae might regulate infected cell detachment induced by hydrogen peroxide that it produces itself, and such a mechanism may contribute to sustaining the bacterial infection.

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Section: Discussionmentioning

confidence: 99%