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Infection and Immunity, February 2008, p. 678-684, Vol. 76, No. 2
0019-9567/08/$08.00+0     doi:10.1128/IAI.00732-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Possible Role for Toll-Like Receptors in Interaction of Fasciola hepatica Excretory/Secretory Products with Bovine Macrophages

Veterinary Sciences Centre, School of Agriculture, Food Science, and Veterinary Medicine, College of Life Sciences, University College Dublin, Belfield, Dublin 4, Ireland

Received 30 May 2007/ Returned for modification 8 September 2007/ Accepted 27 November 2007

Alternative activation of macrophages (M) during helminth infection is a characteristic feature of the host immune response. Alternatively activated macrophages (AAM) are distinguished from others by high arginase 1 (Arg-1) activity, low nitric oxide (NO), and high interleukin 10 (IL-10) production. In murine models, these cells have been shown to possess anti-inflammatory properties. They have also been implicated in exacerbating a subsequent infection with a secondary pathogen. In this study we used cattle experimentally infected with Fasciola hepatica to monitor the kinetics of IL-4 and IL-10 over the course of infection. Using naïve M in vitro, we examined the effects of exposure to F. hepatica excretory/secretory products (FhepES) alone or in combination with IL-4. Our results suggest that FhepES may work in combination with IL-4 to produce AAM. The effects of FhepES on the subsequent responses to lipopolysaccharide (LPS) and purified protein derivative from Mycobacterium bovis (PPD-B), which are bovine Toll-like receptor 4 (TLR4) and TLR2 antagonists, respectively, were also examined. We found that M stimulated with FhepES together with LPS or PPD-B have reduced NO or gamma interferon production, respectively. The ability of FhepES to produce AAM was found to be heat labile and partially dependent on glycan residues. A possible role for TLR recognition is discussed.

Published ahead of print on 10 December 2007.

Editor: J. F. Urban, Jr.