Affiliation:
1. Department of Biomedical Sciences
2. Veterinary Medical Research Institute, Iowa State University, Ames, Iowa 50011
Abstract
ABSTRACT
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
.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Cited by
28 articles.
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