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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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Prif Awduron: Park, Seung-Chun, Yibchok-Anun, Sirintorn, Cheng, Henrique, Young, Theresa F., Thacker, Eileen L., Minion, F. Chris, Ross, Richard F., Hsu, Walter H.
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Cyhoeddwyd: 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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spelling 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
collection PubMed Central
language en
format 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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