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Mesocestoides corti intracranial infection as a murine model for neurocysticercosis

Published online by Cambridge University Press:  29 January 2010

JORGE I. ALVAREZ
Affiliation:
Department of Biology, South Texas Center for Emerging Infectious Diseases, The University of Texas at San Antonio, One UTSA Circle, San Antonio, Texas78249-1644
BIBHUTI B. MISHRA
Affiliation:
Department of Biology, South Texas Center for Emerging Infectious Diseases, The University of Texas at San Antonio, One UTSA Circle, San Antonio, Texas78249-1644
UMA MAHESH GUNDRA
Affiliation:
Department of Biology, South Texas Center for Emerging Infectious Diseases, The University of Texas at San Antonio, One UTSA Circle, San Antonio, Texas78249-1644
PRAMOD K. MISHRA
Affiliation:
Department of Microbiology and Immunology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX, 78229
JUDY M. TEALE*
Affiliation:
Department of Biology, South Texas Center for Emerging Infectious Diseases, The University of Texas at San Antonio, One UTSA Circle, San Antonio, Texas78249-1644 Department of Microbiology and Immunology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX, 78229
*
*Send correspondence and reprint requests to: Judy M. Teale, Ph.D., Department of Biology, The University of Texas at San Antonio, One UTSA Circle, San Antonio, TX78249-1644. Tel: (210) 458-7024. Fax: (210) 458-7025. E-mail: [email protected]

Summary

Neurocysticercosis (NCC) is the most common parasitic disease of the central nervous system (CNS) caused by the larval form of the tapeworm Taenia solium. NCC has a long asymptomatic period with little or no inflammation, and the sequential progression to symptomatic NCC depends upon the intense inflammation associated with degeneration of larvae. The mechanisms involved in these progressive events are difficult to study in human patients. Thus it was necessary to develop an experimental model that replicated NCC. In this review, we describe studies of a murine model of NCC in terms of the release/secretion of parasite antigens, immune responses elicited within the CNS environment and subsequent pathogenesis. In particular, the kinetics of leukocyte subsets infiltrating into the brain are discussed in the context of disruption of the CNS barriers at distinct anatomical sites and the mechanisms contributing to these processes. In addition, production of various inflammatory mediators and the mechanisms involved in their induction by the Toll-like receptor signaling pathway are described. Overall, the knowledge gained from the mouse model of NCC has provided new insights for understanding the kinetics of events contributing to different stages of NCC and should aid in the formulation of more effective therapeutic approaches.

Type
Research Article
Copyright
Copyright © Cambridge University Press 2010

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