Host-parasite interactions in Taenia solium cysticercosis.

A. Clinton White, P. Tato, J. L. Molinari

Research output: Contribution to journalArticle

37 Citations (Scopus)

Abstract

Human neurocysticercosis results from infestation of the central nervous system with the metacestode form (tissue cyst) of Taenia solium. Cysticercosis is being increasingly recognized as a cause of neurologic symptoms in residents and emigrants from developing countries. Taeniid parasites have developed elaborate mechanisms to persist in the tissues of their intermediate hosts. The invasive larvae, termed oncospheres, are susceptible to antibody and complement. However, by the time that the host has generated an antibody response, the parasites have begun to transform to the more resistant metacestode form. The metacestodes also have means of evading complement-mediated destruction, including paramyosin, which inhibits C1q; taeniaestatin, which inhibits both classical and alternate pathways (likely by inhibiting factor D and C3 esterase); and sulfated polysaccharides, which activate complement away from the parasite. Similarly, antibody does not seem to be able to kill the mature metacestode. The parasites may even stimulate the host to produce antibody, which could be bound via Fc receptors, and used as a source of protein. Finally, taeniaestatin and other parasite molecules may interfere with lymphocyte proliferation and macrophage function, thus paralyzing the cellular immune response. Because the symptoms of neurocysticercosis are typically associated with a brisk inflammatory response, we hypothesize that disease is primarily the result of injured or dying parasites. This hypothesis raises important questions in assessing the role of chemotherapy in the management of neurocysticercosis as well as in evaluation of clinical trials, most of which have been uncontrolled.

Original languageEnglish (US)
Pages (from-to)185-193
Number of pages9
JournalInfectious Agents and Disease
Volume1
Issue number4
StatePublished - Aug 1992
Externally publishedYes

Fingerprint

Taenia solium
Cysticercosis
Host-Parasite Interactions
Parasites
Neurocysticercosis
Antibodies
Tropomyosin
Fc Receptors
Esterases
Neurologic Manifestations
Cellular Immunity
Developing Countries
Antibody Formation
Polysaccharides
Larva
Cysts
Central Nervous System
Macrophages
Clinical Trials
Lymphocytes

ASJC Scopus subject areas

  • Microbiology (medical)

Cite this

Host-parasite interactions in Taenia solium cysticercosis. / White, A. Clinton; Tato, P.; Molinari, J. L.

In: Infectious Agents and Disease, Vol. 1, No. 4, 08.1992, p. 185-193.

Research output: Contribution to journalArticle

White, AC, Tato, P & Molinari, JL 1992, 'Host-parasite interactions in Taenia solium cysticercosis.', Infectious Agents and Disease, vol. 1, no. 4, pp. 185-193.
White, A. Clinton ; Tato, P. ; Molinari, J. L. / Host-parasite interactions in Taenia solium cysticercosis. In: Infectious Agents and Disease. 1992 ; Vol. 1, No. 4. pp. 185-193.
@article{45ff3264682f4de4b1dc3391f664fa34,
title = "Host-parasite interactions in Taenia solium cysticercosis.",
abstract = "Human neurocysticercosis results from infestation of the central nervous system with the metacestode form (tissue cyst) of Taenia solium. Cysticercosis is being increasingly recognized as a cause of neurologic symptoms in residents and emigrants from developing countries. Taeniid parasites have developed elaborate mechanisms to persist in the tissues of their intermediate hosts. The invasive larvae, termed oncospheres, are susceptible to antibody and complement. However, by the time that the host has generated an antibody response, the parasites have begun to transform to the more resistant metacestode form. The metacestodes also have means of evading complement-mediated destruction, including paramyosin, which inhibits C1q; taeniaestatin, which inhibits both classical and alternate pathways (likely by inhibiting factor D and C3 esterase); and sulfated polysaccharides, which activate complement away from the parasite. Similarly, antibody does not seem to be able to kill the mature metacestode. The parasites may even stimulate the host to produce antibody, which could be bound via Fc receptors, and used as a source of protein. Finally, taeniaestatin and other parasite molecules may interfere with lymphocyte proliferation and macrophage function, thus paralyzing the cellular immune response. Because the symptoms of neurocysticercosis are typically associated with a brisk inflammatory response, we hypothesize that disease is primarily the result of injured or dying parasites. This hypothesis raises important questions in assessing the role of chemotherapy in the management of neurocysticercosis as well as in evaluation of clinical trials, most of which have been uncontrolled.",
author = "White, {A. Clinton} and P. Tato and Molinari, {J. L.}",
year = "1992",
month = "8",
language = "English (US)",
volume = "1",
pages = "185--193",
journal = "Infectious Agents and Disease",
issn = "1056-2044",
publisher = "Raven Press",
number = "4",

}

TY - JOUR

T1 - Host-parasite interactions in Taenia solium cysticercosis.

AU - White, A. Clinton

AU - Tato, P.

AU - Molinari, J. L.

PY - 1992/8

Y1 - 1992/8

N2 - Human neurocysticercosis results from infestation of the central nervous system with the metacestode form (tissue cyst) of Taenia solium. Cysticercosis is being increasingly recognized as a cause of neurologic symptoms in residents and emigrants from developing countries. Taeniid parasites have developed elaborate mechanisms to persist in the tissues of their intermediate hosts. The invasive larvae, termed oncospheres, are susceptible to antibody and complement. However, by the time that the host has generated an antibody response, the parasites have begun to transform to the more resistant metacestode form. The metacestodes also have means of evading complement-mediated destruction, including paramyosin, which inhibits C1q; taeniaestatin, which inhibits both classical and alternate pathways (likely by inhibiting factor D and C3 esterase); and sulfated polysaccharides, which activate complement away from the parasite. Similarly, antibody does not seem to be able to kill the mature metacestode. The parasites may even stimulate the host to produce antibody, which could be bound via Fc receptors, and used as a source of protein. Finally, taeniaestatin and other parasite molecules may interfere with lymphocyte proliferation and macrophage function, thus paralyzing the cellular immune response. Because the symptoms of neurocysticercosis are typically associated with a brisk inflammatory response, we hypothesize that disease is primarily the result of injured or dying parasites. This hypothesis raises important questions in assessing the role of chemotherapy in the management of neurocysticercosis as well as in evaluation of clinical trials, most of which have been uncontrolled.

AB - Human neurocysticercosis results from infestation of the central nervous system with the metacestode form (tissue cyst) of Taenia solium. Cysticercosis is being increasingly recognized as a cause of neurologic symptoms in residents and emigrants from developing countries. Taeniid parasites have developed elaborate mechanisms to persist in the tissues of their intermediate hosts. The invasive larvae, termed oncospheres, are susceptible to antibody and complement. However, by the time that the host has generated an antibody response, the parasites have begun to transform to the more resistant metacestode form. The metacestodes also have means of evading complement-mediated destruction, including paramyosin, which inhibits C1q; taeniaestatin, which inhibits both classical and alternate pathways (likely by inhibiting factor D and C3 esterase); and sulfated polysaccharides, which activate complement away from the parasite. Similarly, antibody does not seem to be able to kill the mature metacestode. The parasites may even stimulate the host to produce antibody, which could be bound via Fc receptors, and used as a source of protein. Finally, taeniaestatin and other parasite molecules may interfere with lymphocyte proliferation and macrophage function, thus paralyzing the cellular immune response. Because the symptoms of neurocysticercosis are typically associated with a brisk inflammatory response, we hypothesize that disease is primarily the result of injured or dying parasites. This hypothesis raises important questions in assessing the role of chemotherapy in the management of neurocysticercosis as well as in evaluation of clinical trials, most of which have been uncontrolled.

UR - http://www.scopus.com/inward/record.url?scp=0026911140&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026911140&partnerID=8YFLogxK

M3 - Article

VL - 1

SP - 185

EP - 193

JO - Infectious Agents and Disease

JF - Infectious Agents and Disease

SN - 1056-2044

IS - 4

ER -