Journal
SCIENTIFIC REPORTS
Volume 7, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41598-017-12202-z
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Funding
- DGAPA-UNAM [IN-221905, IN-213911, IN-217908]
- CONACYT [70072, 62471-M, 100708, 167278, 106154]
- Fundacion Miguel Aleman
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Taeniids exhibit a great adaptive plasticity, which facilitates their establishment, growth, and reproduction in a hostile inflammatory microenvironment. Transforming Growth Factor-beta (TGF beta), a highly pleiotropic cytokine, plays a critical role in vertebrate morphogenesis, cell differentiation, reproduction, and immune suppression. TGF beta is secreted by host cells in sites lodging parasites. The role of TGF beta in the outcome of T. solium and T. crassiceps cysticercosis is herein explored. Homologues of the TGF beta family receptors (TsRI and TsRII) and several members of the TGF beta downstream signal transduction pathway were found in T. solium genome, and the expression of Type-I and - II TGF beta receptors was confirmed by RT-PCR. Antibodies against TGF beta 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, TGF beta promoted the growth and reproduction of T. crassiceps cysticerci and the survival of T. solium cysticerci. High TGF beta 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 TGF beta in parasite survival. These results indicate the relevance of TGF beta in the infection outcome by promoting cysticercus growth and treatment resistance.
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