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Infection and Immunity, February 2004, p. 1135-1142, Vol. 72, No. 2
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.2.1135-1142.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Platelet-Activating Factor Receptor Deficiency Delays Elimination of Adult Worms but Reduces Fecundity in Strongyloides venezuelensis-Infected Mice

Departamento de Parasitologia,¹ Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais,² Centro de Pesquisas René Rachou-FIOCRUZ, Belo Horizonte, MG, Brazil³

Received 16 July 2003/ Returned for modification 16 August 2003/ Accepted 8 October 2003

We describe the parasitological kinetics and histopathological and immunological alterations in platelet-activating factor receptor-deficient (PAFR^-/-) and wild-type mice after a single Strongyloides venezuelensis infection (subcutaneous inoculation of 500 L3 larvae). There was no difference in the numbers of worms that reached and became established in the small intestines of PAFR^-/- and wild-type mice. However, at 12 days after infection, significantly more worms were recovered from PAFR^-/- mice. Although PAFR^-/- infected mice showed a delay in elimination of adult worms, worms established in the small intestine of these mice produced a significantly lower number of eggs due to a reduction in worm fecundity. There were also significant reductions in the number of circulating and tissue eosinophils and tumor necrosis factor levels in the small intestines of PAFR^-/- mice infected for 7 days compared to the number and level in wild-type mice. Histological analysis confirmed the reduced inflammatory process and revealed that the PAFR^-/- mice had a smaller number of goblet cells. The concentrations of the type 2 cytokines interleukin-4 (IL-4), IL-5, and IL-10 were lower in small intestine homogenates and in supernatants of antigen-stimulated lymphocytes from spleens or mesenteric lymph nodes of PAFR^-/- mice than in the corresponding preparations from wild-type mice. Thus, in S. venezuelensis-infected PAFR^-/- mice, decreased intestinal inflammation is associated with enhanced worm survival but decreased fecundity. We suggest that although a Th2-predominant inflammatory response decreases worm survival, the worm may use factors produced during this response to facilitate egg output and reproduction. PAFR-mediated responses appear to modulate these host-derived signals that are important for worm fecundity.

Editor: W. A. Petri, Jr.

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