Somatostatin negatively regulates parasite burden and granulomatous responses in cysticercosis.

Somatostatin negatively regulates parasite burden and granulomatous responses in cysticercosis.
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生长抑素对囊肿性伴有寄生虫负担和颗粒状反应负调节。

DOI:
10.1155/2014/247182
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发表时间:
2014
影响因子:
--
通讯作者:
Robinson P
Robinson P
中科院分区:
生物学3区
文献类型:
--
作者:
Khumbatta M;Firozgary B;Tweardy DJ;Weinstock J;Firozgary G;Bhatena Z;Bulsara T;Siller R;Robinson P

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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 (P < 0.05). This reduction in parasite burden in SOM−/− mice was accompanied by a 95% increase in size of their granulomas (P < 0.05), which contained a 1.5-fold increase in levels of IFN-γ and a 26-fold decrease in levels of IL-1β (P < 0.05 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.
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发表时间: 2002-08-01
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