Mediators of Inflammation

Mediators of Inflammation / 1993 / Article

Open Access

Volume 2 |Article ID 524738 | https://doi.org/10.1155/S0962935193000109

A. C. Fusco, B. Salafsky, T. Shibuya, "Cytokine and eicosanoid regulation by Schistosoma mansoniduring LSE penetration", Mediators of Inflammation, vol. 2, Article ID 524738, 5 pages, 1993. https://doi.org/10.1155/S0962935193000109

Cytokine and eicosanoid regulation by Schistosoma mansoniduring LSE penetration

Received10 Nov 1992
Accepted08 Dec 1992

Abstract

Cercarial penetration, in low to moderate numbers, does not cause a normal skin inflammatory response; therefore, the authors sought to determine whether cercariae can down-regulate keratinocyte activation and thus the secretion of pro-inflammatory cytokines and eicosanoids. Human living skin equivalent (LSE, Organogenesis) consisting of dermal, epidermal and stratum corneum-like layers was used as the skin substrate. The surface of the LSE membrane was exposed to 100 ng IFNγ or ~850 cercariae for 18 h. Incubation media and tissue was then assayed for IL-1α, IL-6, IL-8, TNFα, 5-HETE, 12-HETE, PGF2, LTB4, and LTC4 via RIA and Western Blots. TNFα was not detected. Secreted IL-1α levels were (mean ± S.E.M. (n)): Control, 1.03 ng ± 0.15 (11); IFNγ 1.90 ng ± 0.48 (5); cercariae, 1.79 ng ± 0.22 (22). In spite of this increase, cercariae down-regulated IL-8 (cercariae 11.13 ± 1.70 ng vs. IFNγ = 16.47 ± 0.29 ng, p = 0.04) and LTB4 (cercariae = 98.86 ± 19.65 pg/0.1 ml vs. IFNγ = 193.42 ± 44.21 pg/0.1 ml p = 0.02). No changes were seen in IL-6, 12-HETE, 5-HETE, and PGE2 levels. It is concluded that cercarial penetration causes a release of IL-1α consistent with skin trauma; however, schistosomulae may regulate the production of chemotactic (neutrophils, macrophages, T-cells, etc.) and activation factors such as IL-8 and LTB4.

Copyright © 1993 Hindawi Publishing Corporation. 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.


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