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Mycoplasma hyopneumoniae Increases Intracellular Calcium Release in Porcine Ciliated Tracheal Cells
We investigated the effects of intact pathogenic Mycoplasma hyopneumoniae, nonpathogenic M. hyopneumoniae, and Mycoplasma flocculare on intracellular free Ca(2+) concentrations ([Ca(2+)](i)) in porcine ciliated tracheal epithelial cells. The ciliated epithelial cells had basal [Ca(2+)](i) of 103 ± 3...
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American Society for Microbiology
2002
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| Mynediad Ar-lein: | https://ncbi.nlm.nih.gov/pmc/articles/PMC127901/ https://ncbi.nlm.nih.gov/pubmed/11953388 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1128/IAI.70.5.2502-2506.2002 |
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pubmed-1279012003-01-08 Mycoplasma hyopneumoniae Increases Intracellular Calcium Release in Porcine Ciliated Tracheal Cells Park, Seung-Chun Yibchok-Anun, Sirintorn Cheng, Henrique Young, Theresa F. Thacker, Eileen L. Minion, F. Chris Ross, Richard F. Hsu, Walter H. Infect Immun Cellular Microbiology: Pathogen-Host Cell Molecular Interactions We investigated the effects of intact pathogenic Mycoplasma hyopneumoniae, nonpathogenic M. hyopneumoniae, and Mycoplasma flocculare on intracellular free Ca(2+) concentrations ([Ca(2+)](i)) in porcine ciliated tracheal epithelial cells. The ciliated epithelial cells had basal [Ca(2+)](i) of 103 ± 3 nM (n = 217 cells). The [Ca(2+)](i) increased by 250 ± 19 nM (n = 47 cells) from the basal level within 100 s of the addition of pathogenic M. hyopneumoniae strain 91-3 (300 μg/ml), and this increase lasted ∼60 s. In contrast, nonpathogenic M. hyopneumoniae and M. flocculare at concentrations of 300 μg/ml failed to increase [Ca(2+)](i). In Ca(2+)-free medium, pathogenic M. hyopneumoniae still increased [Ca(2+)](i) in tracheal cells. Pretreatment with thapsigargin (1 μM for 30 min), which depleted the Ca(2+) store in the endoplasmic reticulum, abolished the effect of M. hyoneumoniae. Pretreatment with pertussis toxin (100 ng/ml for 3 h) or U-73122 (2 μM for 100 s), an inhibitor of phospholipase C, also abolished the effect of M. hyopneumoniae. The administration of mastoparan 7, an activator of pertussis toxin-sensitive proteins G(i) and G(o), increased [Ca(2+)](i) in ciliated tracheal cells. These results suggest that pathogenic M. hyopneumoniae activates receptors that are coupled to G(i) or G(o), which in turn activates a phospholipase C pathway, thereby releasing Ca(2+) from the endoplasmic reticulum. Thus, an increase in Ca(2+) may serve as a signal for the pathogenesis of M. hyopneumoniae. American Society for Microbiology 2002-05 /pmc/articles/PMC127901/ /pubmed/11953388 http://dx.doi.org/10.1128/IAI.70.5.2502-2506.2002 Text en Copyright © 2002, American Society for Microbiology |
| institution |
US National Library of Medicine |
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PubMed Central |
| language |
en |
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Article |
| topic |
Cellular Microbiology: Pathogen-Host Cell Molecular Interactions |
| spellingShingle |
Cellular Microbiology: Pathogen-Host Cell Molecular Interactions Park, Seung-Chun Yibchok-Anun, Sirintorn Cheng, Henrique Young, Theresa F. Thacker, Eileen L. Minion, F. Chris Ross, Richard F. Hsu, Walter H. Mycoplasma hyopneumoniae Increases Intracellular Calcium Release in Porcine Ciliated Tracheal Cells |
| description |
We investigated the effects of intact pathogenic Mycoplasma hyopneumoniae, nonpathogenic M. hyopneumoniae, and Mycoplasma flocculare on intracellular free Ca(2+) concentrations ([Ca(2+)](i)) in porcine ciliated tracheal epithelial cells. The ciliated epithelial cells had basal [Ca(2+)](i) of 103 ± 3 nM (n = 217 cells). The [Ca(2+)](i) increased by 250 ± 19 nM (n = 47 cells) from the basal level within 100 s of the addition of pathogenic M. hyopneumoniae strain 91-3 (300 μg/ml), and this increase lasted ∼60 s. In contrast, nonpathogenic M. hyopneumoniae and M. flocculare at concentrations of 300 μg/ml failed to increase [Ca(2+)](i). In Ca(2+)-free medium, pathogenic M. hyopneumoniae still increased [Ca(2+)](i) in tracheal cells. Pretreatment with thapsigargin (1 μM for 30 min), which depleted the Ca(2+) store in the endoplasmic reticulum, abolished the effect of M. hyoneumoniae. Pretreatment with pertussis toxin (100 ng/ml for 3 h) or U-73122 (2 μM for 100 s), an inhibitor of phospholipase C, also abolished the effect of M. hyopneumoniae. The administration of mastoparan 7, an activator of pertussis toxin-sensitive proteins G(i) and G(o), increased [Ca(2+)](i) in ciliated tracheal cells. These results suggest that pathogenic M. hyopneumoniae activates receptors that are coupled to G(i) or G(o), which in turn activates a phospholipase C pathway, thereby releasing Ca(2+) from the endoplasmic reticulum. Thus, an increase in Ca(2+) may serve as a signal for the pathogenesis of M. hyopneumoniae. |
| author |
Park, Seung-Chun Yibchok-Anun, Sirintorn Cheng, Henrique Young, Theresa F. Thacker, Eileen L. Minion, F. Chris Ross, Richard F. Hsu, Walter H. |
| author_facet |
Park, Seung-Chun Yibchok-Anun, Sirintorn Cheng, Henrique Young, Theresa F. Thacker, Eileen L. Minion, F. Chris Ross, Richard F. Hsu, Walter H. |
| author_sort |
Park, Seung-Chun |
| title |
Mycoplasma hyopneumoniae Increases Intracellular Calcium Release in Porcine Ciliated Tracheal Cells |
| title_short |
Mycoplasma hyopneumoniae Increases Intracellular Calcium Release in Porcine Ciliated Tracheal Cells |
| title_full |
Mycoplasma hyopneumoniae Increases Intracellular Calcium Release in Porcine Ciliated Tracheal Cells |
| title_fullStr |
Mycoplasma hyopneumoniae Increases Intracellular Calcium Release in Porcine Ciliated Tracheal Cells |
| title_full_unstemmed |
Mycoplasma hyopneumoniae Increases Intracellular Calcium Release in Porcine Ciliated Tracheal Cells |
| title_sort |
mycoplasma hyopneumoniae increases intracellular calcium release in porcine ciliated tracheal cells |
| publisher |
American Society for Microbiology |
| publisher_facet |
American Society for Microbiology |
| publishDate |
2002 |
| url |
https://ncbi.nlm.nih.gov/pmc/articles/PMC127901/ https://ncbi.nlm.nih.gov/pubmed/11953388 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1128/IAI.70.5.2502-2506.2002 |
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1759033894615646208 |