Hemolysin of
            <i>Mycoplasma pneumoniae</i>
            : Tentative Identification as a Peroxide

Somerson, Norman L.; Walls, Barbara E.; Chanock, Robert M.

doi:10.1126/science.150.3693.226

Cited by 94 publications

(54 citation statements)

References 11 publications

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“…Based on previous reports (8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(39)(40)(41)(42) and on the data presented in our study, the following pathogenetic events ofM. pneumoniae infection are suggested (Fig.…”

Section: Discussionsupporting

confidence: 70%

Role of superoxide anion in host cell injury induced by mycoplasma pneumoniae infection. A study in normal and trisomy 21 cells.

Almagor¹,

Kahane²,

Yatziv³

1984

J. Clin. Invest.

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Abstract. The role ofMycoplasma pneumoniaegenerated superoxide and hydrogen peroxide in inducing host cell injury was studied in normal and trisomy 21 human cells. As a result of M. pneumoniae infection, catalase activity in infected normal skin fibroblasts and ciliated epithelial cells decreased by 74-77% as compared with uninfected controls. Addition of superoxide dismutase to the infected cultured cells totally prevented the inhibition whereas addition of catalase or catalytically inactivated superoxide dismutase had no protective effect. Trisomy 21 erythrocytes and cultured skin fibroblasts in which CuZn-superoxide dismutase content is 50% greater than in normal cells were infected by M. pneumoniae. The inhibition of catalase activity in these cells was 7-33% and 0-20.5%, respectively, as compared with 65-72% and 48-68% inhibition in normal infected controls. Following M. pneumoniae infection, the levels of malonyldialdehyde, an indicator for membrane lipid peroxidation were raised in trisomy 21 cultured fibroblasts by 10-32% while in normal cells malonyldialdehyde increased by 140-870%. Externally added superoxide dismutase, but not catalase, reduced the extent of lipid peroxidation in normal infected cells. Lactate dehydrogenase release from normal infected cells was time correlated with the increase in their malonyldialdehyde formation. It is suggested that superoxide generated during M. pneumoniae infection is involved in the inhibition of host cell catalase activity. The inactivation of this cellular antioxReceivedfor publication 9 August 1983 and in revisedform 24 October 1983. idative defense mechanism results in progressive oxidative damage to the M. pneumoniae-infected cells.

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Section: Discussionsupporting

confidence: 70%

Role of superoxide anion in host cell injury induced by mycoplasma pneumoniae infection. A study in normal and trisomy 21 cells.

Almagor¹,

Kahane²,

Yatziv³

1984

J. Clin. Invest.

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“…Virulence mechanisms in the pathogenicity of mycoplasma infection have been related to the generation of various products, including exotoxins (9), phospholipases (39,40,45), proteases (37), and urease (26), and to oxidative damage (43). Different groups have also reported that host DNA and RNA represent a potential target for membrane-associated and/or exported nucleases from mycoplasmas.…”

Section: Discussionmentioning

confidence: 99%

Purification and characterization of Mycoplasma penetrans Ca2+/Mg2+-dependent endonuclease

et al. 1997

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The major nuclease from Mycoplasma penetrans has been purified to homogeneity. The enzyme seems to be present as a membrane-associated precursor of 50 kDa and as a peripheral membrane monomeric polypeptide of 40 kDa that is easily removed by washing of cells with isotonic buffers and in the aqueous phase upon , heparin, sodium dodecyl sulfate, and chelator agents such EDTA and EGTA, but no effect was observed with ATP, 2-mercaptoethanol, N-ethylmaleimide, dithiothreitol, nonionic detergents, phenylmethylsulfonyl fluoride, and iodoacetamide. Nuclease activity was inhibited by diethylpyrocarbonate at both pH 6 and 8 and by pepstatin, suggesting the involvement of a histidine and an aspartate in the active site. When added to human lymphoblast nuclei, the purified M. penetrans endonuclease induced internucleosomal fragmentation of the chomatin into oligonucleosomal fragments. On the basis of this result, and taking into account the fact that M. penetrans has the capacity to invade eucaryotic cells, one can suggest, but not assert, that produced Ca 2؉ /Mg 2؉

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“…The hemolytic activity of M. pneumoniae is due to production of H 2 O 2 and is inhibited by catalase (264). In contrast, the hemolytic activity of ureaplasmas is not inhibited by catalase, suggesting an alternative enzyme system may be responsible (96).…”

Section: Secretory Productsmentioning

confidence: 99%

Mycoplasmas and Ureaplasmas as Neonatal Pathogens

Katz²,

2005

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SUMMARY The genital mycoplasmas represent a complex and unique group of microorganisms that have been associated with a wide array of infectious diseases in adults and infants. The lack of conclusive knowledge regarding the pathogenic potential of Mycoplasma and Ureaplasma spp. in many conditions is due to a general unfamiliarity of physicians and microbiology laboratories with their fastidious growth requirements, leading to difficulty in their detection; their high prevalence in healthy persons; the poor design of research studies attempting to base association with disease on the mere presence of the organisms in the lower urogenital tract; the failure to consider multifactorial aspects of diseases; and considering these genital mycoplasmas only as a last resort. The situation is now changing because of a greater appreciation of the genital mycoplasmas as perinatal pathogens and improvements in laboratory detection, particularly with regard to the development of powerful molecular nucleic acid amplification tests. This review summarizes the epidemiology of genital mycoplasmas as causes of neonatal infections and premature birth; evidence linking ureaplasmas with bronchopulmonary dysplasia; recent changes in the taxonomy of the genus Ureaplasma; the neonatal host response to mycoplasma and ureaplasma infections; advances in laboratory detection, including molecular methods; and therapeutic considerations for treatment of systemic diseases.

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Hemolysin of Mycoplasma pneumoniae : Tentative Identification as a Peroxide

Cited by 94 publications

References 11 publications

Role of superoxide anion in host cell injury induced by mycoplasma pneumoniae infection. A study in normal and trisomy 21 cells.

Role of superoxide anion in host cell injury induced by mycoplasma pneumoniae infection. A study in normal and trisomy 21 cells.

Purification and characterization of Mycoplasma penetrans Ca2+/Mg2+-dependent endonuclease

Mycoplasmas and Ureaplasmas as Neonatal Pathogens

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