Pathogenicity Factors in Mycoplasmas and Spiroplasmas

Gabridge, Michael G.; Chandler, D. K. F.; Daniels, Michael J.

doi:10.1016/b978-0-12-078404-2.50016-6

Cited by 16 publications

(24 citation statements)

References 187 publications

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“…Although both lipopolysaccharide and M. caprieolum membranes activate macrophages to secrete TNF« and kill tumor target cells, the absence of lipopolysaccharide in M. eapricolum membranes [31] suggests that mycoplasma membranes operate via a different mechanism. It should be noted that in several mycoplasmas, mainly Aeholeplasma species, a unique lipid-polysaccharide molecule, named lipoglycan, has been detected in the cell membrane [14]. The lipoglycan was, however, incapable of inducing macrophage-mediated cytolysis [34].…”

Section: Discussionmentioning

confidence: 99%

“…The mechanism responsible for lipopolysaccharide-induced endotoxic shock remains unclear, although it has been postulated that several factors, including TNF«, may mediate this process [2,19]. In the present study we investigated the possibility that Mycoplasma capricolum, a nontoxic mycoplasma [14] that lacks lipopolysaccharide [31], could be substituted for lipopolysaccharide to induce TNFc~ production. Preliminary evidence that mycoplasmas activate normal mouse peritoneal macrophages to become both cytotoxic to target cells and to exhibit enhanced bacteriocidal capacities against intracellular pathogens were presented by Hibbs [17], using M. arginini and M. pulmonis.…”

Section: Introductionmentioning

confidence: 99%

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Mycoplasma capricolum membranes induce tumor necrosis factor α by a mechanism different from that of lipopolysaccharide

Sher

Rottem

Gallily

1990

Cancer Immunol Immunother

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Heat-inactivated (60 degrees C, 45 min) Mycoplasma capricolum strain JR cells activate murine macrophages to secrete high levels of tumor necrosis factor alpha (TNF alpha) and to lyse tumor target cells efficiently. Fractionation of the intact M. capricolum cells, obtained from cells harvested at the exponential phase of growth, shows that their capacity to induce TNF alpha secretion by macrophage resides exclusively in the membrane fraction. The macrophage-mediated cytolysis following activation by M. capricolum membranes was significantly inhibited by specific anti-recombinant murine TNF alpha antibodies. M. capricolum membranes are a potent inducer of TNF alpha as the commonly used bacterial lipopolysaccharide, indicated by their dose-response curve for macrophage activation. Our study further showed that M. capricolum membranes and lipopolysaccharide synergize to augment TNF alpha secretion by C57BL/6-derived macrophages markedly. Moreover, lipopolysaccharide-unresponsive C3H/HeJ-derived macrophages, were pronouncedly activated by M. capricolum membranes, which do not contain lipopolysaccharide. These findings suggest that the mechanism by which M. capricolum membranes activate macrophages differs from that of lipopolysaccharide. Results of preliminary experiments show that human monocytes as well secrete TNF alpha following activation by M. capricolum membranes. Thus, in contrast with the prohibitive toxicity of lipopolysaccharide to animals and humans, M. capricolum membranes, which contain no lipopolysaccharide and are nontoxic in nature, may be of therapeutic value in the treatment of cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mycoplasma capricolum membranes induce tumor necrosis factor α by a mechanism different from that of lipopolysaccharide

Sher

Rottem

Gallily

1990

Cancer Immunol Immunother

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“…Inhaled pollutants such as ozone (03), nitrogen dioxide, automobile exhaust, and cigarette smoke contain numerous oxidants (3). Aerobic bacteria produce ROS; those which are catalase negative (e.g., Mycoplasma pneumoniae) can be an additional source of exogenous H202 in infected airways (4). Phagocytic cells, a first line of defense against microorganisms, produce superoxide anions and related products (H202, HOCI, OH*) (5).…”

Section: Introductionmentioning

confidence: 99%

Interactions of oxygen radicals with airway epithelium.

Wright

Cohn

et al. 1994

Environ Health Perspect

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Reactive oxygen species (ROS) have been implicated in the pathogenesis of numerous disease processes. Epithelial cells lining the respiratory airways are uniquely vulnerable regarding potential for oxidative damage due to their potential for exposure to both endogenous (e.g., mitochondrial respiration, phagocytic respiratory burst, cellular oxidases) and exogenous (e.g., air pollutants, xenobiotics, catalase negative organisms) oxidants. Airway epithelial cells use several nonenzymatic and enzymatic antioxidant mechanisms to protect against oxidative insult. Nonenzymatic defenses include certain vitamins and low molecular weight compounds such as thiols. The enzymes superoxide dismutase, catalase, and glutatione peroxidase are major sources of antioxidant protection. Other materials associated with airway epithelium such as mucus, epithelial lining fluid, and even the basement membrane/extracellular matrix may have protective actions as well. When the normal balance between oxidants and antioxidants is upset, oxidant stress ensues and subsequent epithelial cell alterations or damage may be a critical component in the pathogenesis of several respiratory diseases. Oxidant stress may profoundly alter lung physiology including pulmonary function (e.g., forced expiratory volumes, flow rates, and maximal inspiratory capacity), mucociliary activity, and airway reactivity. ROS may induce airway inflammation; the inflammatory process may serve as an additional source of ROS in airways and provoke the pathophysiologic responses described. On a more fundamental level, cellular mechanisms in the pathogenesis of ROS may involve activation of intracellular signaling enzymes including phospholipases and protein kinases stimulating the release of inflammatory lipids and cytokines. Respiratory epithelium may be intimately involved in defense against, and pathophysiologic changes invoked by, ROS. -Environ Health Perspect 1 02(Suppl 1 0): 85-90 (1994)

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“…As a result some pathogenic mycoplasmas have evolved a specialized attachment organelle (Gabridge et al, 1985). The specialized attachment proteins of M. pneumoniae and Af, gallisepticum have been studied extensively and the major cytadhesin gene of M.…”

Section: Genetic Approaches To Studying Mycoplasma Diseasesmentioning

confidence: 99%

“…The pathogenic mechanisms of mycoplasmas remain a paradox because with one exception, no extracellular products or toxins have been identified (Gabridge et al, 1985). Instead, mycoplasmas appear to induce metabolic and moiphological changes in host cells through subtle chemical processes (Gabridge et al, 1985).…”

Section: Genetic Approaches To Studying Mycoplasma Diseasesmentioning

confidence: 99%

Development of molecular genetic approaches to study mycoplasma pathogenesis

Mahairas

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Rogers et al., 1985;Woese, 1985). Rifampin sensitivity, a general property of eubacterial DNA-dependent RNA polymerases (Sippel and Hartman, 1968), also provided supportive evidence of the 3 phylogenetic relationships. Rifampin acts on the P subunit of the RNA polymerase holoenzyme to inhibit the initiation step of transcription (Rabussay and Zillig, 1969). Gadeau et al. (1986) show that the growth of five representative Mollicutes was insensitive to rifampin in contrast to E. coli which was fully inhibited. Additional evidence was provided by in vitro experiments that showed that S. apis and S. melliferim enzymes were rifampin resistant even though their subunit structure strongly resembled that of E. coli (Gadeau et al., 1986).Interestingly, the RNA polymerase of A. laidlawii showed a marked sensitivity to rifampin as compared with the Spiroplasma enzymes but there was a greater degree of resistance than with the E. coli enzyme (Gadeau et al., 1986). Therefore it is believed that the sensitivity to rifampin was lost during the splitting of the Acholeplasma branch of the phylogenetic tree.The Mycoplasma GenomeThe tRNA species. The M. capricolum genome also contained two sets of rRNA genes compared to the ten sets of Bacillus subtilis (Widom et al., 1988).All species of the Mollicutes have a relatively low G + C content although a large variation exists (Razin and Freundt, 1984). The G + C content of all species of Ureaplasma was reported to be about 28% while that of most organisms in the genus Mycoplasma was between 24-30% (Razin and Freundt, 1984). It should be noted that the G + C content of M.gallisepticum was 32% while that of M. pneumoniae was about 38% (Razin and Freundt, 1984). These organisms are the prototypes of a small group of higher G + C mycoplasmas (Razin and Freundt, 1984). Halden et al., 1989). iSc/Nl is an isoschizomer of Hhal that recognizes the sequence 5'-GCGC-3' (Stephens, 1982) cleaving between the first G and C generating a two base 5' , 1985).A system to generate energy from ATP is also required for autonomous growth.Schiefer and Schummer (1982) examined several mycoplasmas and found that energy is generated by a membrane bound proton-translocating adenosine triphosphatase that hydrolyzes ATP formed in glycolysis leading to proton extrusion. Additionally, Zilberstein et al. (1986) showed that the FIFQ ATPase of several mycoplasmas were immunologically crossreactive with that of E. coli in the active site region but differed in that the mycoplasma enzymes had an altered structure and were covalently anchored to the membrane. About 270 genes in the E.coli genome encode components of the protein and nucleic acid synthesizing machinery, including RNA and DNA polymerases, ribosomal proteins, tRNAs and additional transcription and translation factors (Muto, 1987). Thus it is thought that in the mycoplasmas, a major portion of the coding regions is devoted to these essential functions as well as the generation of energy making the mycoplasmas the minimal information coding for a livi...

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Pathogenicity Factors in Mycoplasmas and Spiroplasmas

Cited by 16 publications

References 187 publications

Mycoplasma capricolum membranes induce tumor necrosis factor α by a mechanism different from that of lipopolysaccharide

Mycoplasma capricolum membranes induce tumor necrosis factor α by a mechanism different from that of lipopolysaccharide

Interactions of oxygen radicals with airway epithelium.

Development of molecular genetic approaches to study mycoplasma pathogenesis

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