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Infection and Immunity, May 2002, p. 2502-2506, Vol. 70, No. 5
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.5.2502-2506.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Mycoplasma hyopneumoniae Increases Intracellular Calcium Release in Porcine Ciliated Tracheal Cells

Seung-Chun Park,^1, Sirintorn Yibchok-Anun,^1, Henrique Cheng,¹ Theresa F. Young,² Eileen L. Thacker,² F. Chris Minion,² Richard F. Ross,² and Walter H. Hsu^1*

Department of Biomedical Sciences,¹ Veterinary Medical Research Institute, Iowa State University, Ames, Iowa 50011²

Received 3 August 2001/ Returned for modification 20 November 2001/ Accepted 30 January 2002

We investigated the effects of intact pathogenic Mycoplasma hyopneumoniae, nonpathogenic M. hyopneumoniae, and Mycoplasma flocculare on intracellular free Ca²⁺ concentrations ([Ca²⁺]_i) in porcine ciliated tracheal epithelial cells. The ciliated epithelial cells had basal [Ca²⁺]_i of 103 ± 3 nM (n = 217 cells). The [Ca²⁺]_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 [Ca²⁺]_i. In Ca²⁺-free medium, pathogenic M. hyopneumoniae still increased [Ca²⁺]_i in tracheal cells. Pretreatment with thapsigargin (1 µM for 30 min), which depleted the Ca²⁺ 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 [Ca²⁺]_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 Ca²⁺ from the endoplasmic reticulum. Thus, an increase in Ca²⁺ may serve as a signal for the pathogenesis of M. hyopneumoniae.

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* Corresponding author. Mailing address: Department of Biomedical Sciences, Iowa State University, Ames, IA 50011. Phone: (515) 294-6864. Fax: (515) 294-2315. E-mail: whsu{at}iastate.edu.

Editor: V. J. DiRita

Present address: Department of Veterinary Pharmacology & Toxicology, College of Veterinary Medicine, Kyungpook National University, Taegu 702-701, Republic of Korea.

Present address: Department of Veterinary Pharmacology, Faculty of Veterinary Science, Chulalongkorn University, Bangkok 10330, Thailand.

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Infection and Immunity, May 2002, p. 2502-2506, Vol. 70, No. 5
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.5.2502-2506.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

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