Abstract
Taeniids exhibit a great adaptive plasticity, which facilitates their establishment, growth, and reproduction in a hostile inflammatory microenvironment. Transforming Growth Factor-β (TGFβ), a highly pleiotropic cytokine, plays a critical role in vertebrate morphogenesis, cell differentiation, reproduction, and immune suppression. TGFβ is secreted by host cells in sites lodging parasites. The role of TGFβ in the outcome of T. solium and T. crassiceps cysticercosis is herein explored. Homologues of the TGFβ family receptors (TsRI and TsRII) and several members of the TGFβ downstream signal transduction pathway were found in T. solium genome, and the expression of Type-I and -II TGFβ receptors was confirmed by RT-PCR. Antibodies against TGFβ family receptors recognized cysticercal proteins of the expected molecular weight as determined by Western blot, and different structures in the parasite external tegument. In vitro, TGFβ promoted the growth and reproduction of T. crassiceps cysticerci and the survival of T. solium cysticerci. High TGFβ levels were found in cerebrospinal fluid from untreated neurocysticercotic patients who eventually failed to respond to the treatment (P = 0.03) pointing to the involvement of TGFβ in parasite survival. These results indicate the relevance of TGFβ in the infection outcome by promoting cysticercus growth and treatment resistance.
Highlights
Taenia solium is a parasite whose larval stage may locate in the human central nervous system, causing neurocysticercosis (NC) a disease prevalent in developing countries
These findings suggest a relevant role for this growth factor in the host-parasite relationship
Genes coding for proteins of the Transforming Growth Factor-β (TGFβ) signaling pathway were searched in T. solium genome; their functional impact on the host-parasite relationship in cysticercosis was studied by measuring their capacity to modulate the growth and survival of T. crassiceps and T. solium cysticerci
Summary
Taenia solium is a parasite whose larval stage (cysticercus) may locate in the human central nervous system, causing neurocysticercosis (NC) a disease prevalent in developing countries. It has been observed that some helminths have the potential to produce TGFβ family products (Activin and Bone morphogenetic protein)[6,13,14,15] and several of the TGFβ signaling pathways factors have been found in the genome of these parasites[16]. Overall, these findings suggest a relevant role for this growth factor in the host-parasite relationship. This work explores the possible involvement of TGFβ in the resistance to cysticidal treatment in severe NC human patients
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