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BioMed Research International
Volume 2014 (2014), Article ID 247182, 6 pages
Research Article

Somatostatin Negatively Regulates Parasite Burden and Granulomatous Responses in Cysticercosis

1Section of Infectious Diseases, Department of Medicine, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA
2Division of Gastroenterology, Department of Medicine, Tufts Medical Center, 800 Washington Street, P.O. Box 233, Boston, MA 02111, USA

Received 1 April 2014; Revised 3 June 2014; Accepted 4 June 2014; Published 9 July 2014

Academic Editor: Luis I. Terrazas

Copyright © 2014 Mitra Khumbatta et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Cysticercosis is an infection of tissues with the larval cysts of the cestode, Taenia  solium. While live parasites elicit little or no inflammation, dying parasites initiate a granulomatous reaction presenting as painful muscle nodules or seizures when cysts are located in the brain. We previously showed in the T. crassiceps murine model of cysticercosis that substance P (SP), a neuropeptide, was detected in early granulomas and was responsible for promoting granuloma formation, while somatostatin (SOM), another neuropeptide and immunomodulatory hormone, was detected in late granulomas; SOM’s contribution to granuloma formation was not examined. In the current studies, we used somatostatin knockout (SOM−/−) mice to examine the hypothesis that SOM downmodulates granulomatous inflammation in cysticercosis, thereby promoting parasite growth. Our results demonstrated that parasite burden was reduced 5.9-fold in SOM−/− mice compared to WT mice (). This reduction in parasite burden in SOM−/− mice was accompanied by a 95% increase in size of their granulomas (), which contained a 1.5-fold increase in levels of IFN-γ and a 26-fold decrease in levels of IL-1β ( for both) compared to granulomas from WT mice. Thus, SOM regulates both parasite burden and granulomatous inflammation perhaps through modulating granuloma production of IFN-γ and IL-1β.