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Infection and Immunity, April 1999, p. 1547-1552, Vol. 67, No. 4
Departments of
Medicine1 and
Pathology,2 University of California,
San Diego, San Diego, California 92103-8416
Received 12 August 1998/Returned for modification 16 September
1998/Accepted 5 January 1999
The ubiquitous protozoan parasite Toxoplasma gondii is
a major cause of morbidity and mortality in neonates and
immunocompromised hosts. Both acute invasion and reactivation of latent
infection result in an inflammatory reaction with lymphocytes,
macrophages, and neutrophils. The mechanisms responsible for triggering
the local host response to toxoplasmosis are not fully understood. Infection of monolayers of human HeLa epithelial cells and fibroblasts with T. gondii resulted in a marked increase in the
expression of interleukin-8 (IL-8)-specific mRNA and secretion of the
proinflammatory and chemoattractant cytokines interleukin-8 (IL-8),
GRO
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Chemokine Secretion of Human Cells in Response to
Toxoplasma gondii Infection
, and MCP-1. Host cell invasion and lysis were required for this
response, as tachyzoite lysates alone had no effect on IL-8 secretion.
IL-8 release was dependent on the release of soluble host cell factors: IL-1
in HeLa cells and an additional mediator in fibroblasts. HT-29
epithelial cells, which lack IL-1
or another IL-8-inducing activity,
did not release IL-8 after infection, although they were efficiently
infected with T. gondii and increased IL-8 secretion in
response to added IL-1
. These data suggest that proinflammatory chemokine secretion is an important host cell response to toxoplasmosis and that the release of IL-1
and other mediators from lysed host cells is critical for this chemokine response.
*
Corresponding author. Mailing address: Division of
Infectious Diseases, UCSD Medical Center, 200 W. Arbor Dr., San Diego, CA 92103-8416. Phone: (619) 543-6146. Fax: (619) 543-6614. E-mail: slreed{at}popmail.ucsd.edu.
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