Mycoplasma penetrans

Mycoplasma penetrans is a species of Gram-positive bacteria.[1][2] It is pathogenic, though many infected show no symptoms. It is a sexually transmitted disease, though an infant may be infected during birth.[3][4]

Mycoplasma penetrans
Scientific classification
Domain: Bacteria
Phylum: Mycoplasmatota
Class: Mollicutes
Order: Mycoplasmatales
Family: Mycoplasmataceae
Genus: Mycoplasma
Species:
M. penetrans
Binomial name
Mycoplasma penetrans
Lo et al. 1992

Description

It has an elongated shape and its cells possess two internal compartments, one packed with granules, the other filled with coarse granules (consistent with ribosomal structures). The organism has properties of adherence through a specific organelle called the tip organelle. M. Penetrans has a coding sequence (MYPE1570) similar to that of MYPE470 in Mycoplasma pneumoniae which codes for an accessory protein that aids in cytadherence,[5] the adherence to respiratory epithelium. This similarity suggests M. penetrans could attach to host cells through cytadherence. Also, the CDS MYPE1550, which is near MYPE1570, of M. penetrans is orthologous to the hemadsorption protein HMW2 of M pneumoniae, suggesting the potential for M. penetrans to attach to and invade red blood cells.[5]

Virulence factors

Mycoplasma penetrans, like many bacteria, exhibits a mechanism by which it can avoid an immune response in the host cells. This avoidance of immune responses is known as a virulence factor. The virulence factor that M. penetrans displays is antigenic variation, the ability to exchange or switch antigens against which the host cell produces antibodies. The mpl gene encodes for the bacteria's antigens and, like most genes, it contains a promoter region. In M. penetrans, this promoter region can undergo reversible inversion, allowing for variation in antigen production and, thus, the source for M. penetrans antigenic variation.[6]

Diseases

Mycoplasma penetrans has been shown to hinder p53, a tumor suppressing gene that aids in regulating the cell cycle.[7] There have also been cases of malignant pleural effusion, when patients exhibited chronic M. penetrans infection with various immunodeficiencies (such as HIV infections or anticancer treatment).[8] This particular species is also a sexually transmitted disease and one cause of pelvic inflammatory disease.[9]

References
  1. Gallego, Pablo; Planell, Raquel; Benach, Jordi; Querol, Enrique; Perez-Pons, Joseph A.; Reverter, David (October 17, 2012). "Structural Characterization of the Enzymes Composing the Arginine Deiminase Pathway in Mycoplasma penetrans". PLOS ONE. 7 (10): e47886. Bibcode:2012PLoSO...747886G. doi:10.1371/journal.pone.0047886. PMC 3474736. PMID 23082227. Retrieved 11 November 2014.
  2. Lo, S.-C.; Hayes, M. M.; Tully, J. G.; Wang, R. Y.-H.; Kotani, H.; Pierce, P. F.; Rose, D. L.; Shih, J. W.-K. (1992). "Mycoplasma penetrans sp. nov., from the Urogenital Tract of Patients with AIDS". International Journal of Systematic Bacteriology. 42 (3): 357–364. doi:10.1099/00207713-42-3-357. ISSN 0020-7713. PMID 1503969.
  3. Yáñez A, Cedillo L, Neyrolles O, et al. (1999). "Mycoplasma penetrans bacteremia and primary antiphospholipid syndrome". Emerging Infectious Diseases. 5 (1): 164–7. doi:10.3201/eid0501.990122. PMC 2627698. PMID 10081687.
  4. Ljubin-Sternak, Sunčanica; Meštrović, Tomislav (2014). "Chlamydia trachomatis and Genital Mycoplasmas: Pathogens with an Impact on Human Reproductive Healthogens with an Impact on Human Reproductive Health". Journal of Pathogens. 2014: 183167. doi:10.1155/2014/183167. PMC 4295611. PMID 25614838.
  5. Sasaki, Y.; Ishikawa, J.; Yamashita, A.; Oshima, K.; Kenri, T.; Furuya, K.; Hattori, M (2002-12-01). "The complete genomic sequence of Mycoplasma penetrans, an intracellular bacterial pathogen in humans". Nucleic Acids Research. 30 (23): 5293–5300. doi:10.1093/nar/gkf667. ISSN 1362-4962. PMC 137978. PMID 12466555.
  6. Horino, A.; Sasaki, Y.; Sasaki, T.; Kenri, T. (2003-01-01). "Multiple Promoter Inversions Generate Surface Antigenic Variation in Mycoplasma penetrans". Journal of Bacteriology. 185 (1): 231–242. doi:10.1128/jb.185.1.231-242.2003. ISSN 0021-9193. PMC 141813. PMID 12486060.
  7. Logunov, D Y; Scheblyakov, D V; Zubkova, O V; Shmarov, M M; Rakovskaya, I V; Gurova, K V; Tararova, N D; Burdelya, L G; Naroditsky, B S (2008-04-14). "Mycoplasma infection suppresses p53, activates NF-κB and cooperates with oncogenic Ras in rodent fibroblast transformation". Oncogene. 27 (33): 4521–4531. doi:10.1038/onc.2008.103. ISSN 0950-9232. PMC 4526267. PMID 18408766.
  8. Cao, Shuyan; Shen, Dandan; Wang, Yadong; Li, Linxi; Zhou, Liping; Wang, Yuxue (2017-07-10). "Potential malignant transformation in the gastric mucosa of immunodeficient mice with persistent Mycoplasma penetrans infection". PLOS ONE. 12 (7): e0180514. Bibcode:2017PLoSO..1280514C. doi:10.1371/journal.pone.0180514. ISSN 1932-6203. PMC 5503272. PMID 28692662.
  9. Ljubin-Sternak, Suncanica; Mestrovic, Tomislav (2014). "Review: Chlamydia trachonmatis and Genital Mycoplasmias: Pathogens with an Impact on Human Reproductive Health". Journal of Pathogens. 2014 (183167): 183167. doi:10.1155/2014/183167. PMC 4295611. PMID 25614838.

Further reading
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