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Since the publication of the mouse genome, attention has focused on the strains that were selected for sequencing. In this paper we report the results of experiments that characterized the response to infection with the murine gastrointestinal nematode Heligmosomoides polygyrus of eight new strains (A/J, C57BL/6, C3H, DBA/2, BALB/c, NIH, SJL and 129/J), in addition to the well-characterized CBA (poor responder) and SWR (strong responder) as our controls. We employed the repeated infection protocol (consisting of 7 superimposed doses of 125L3 each administered at weekly intervals, faecal egg counts in weeks 2, 4 and 6 and assessment of worm burdens in week 6) that was used successfully to identify quantitative trait loci for genes involved in resistance to H. polygyrus . SWR, SJL and NIH mice performed indistinguishably and are confirmed as strong responder strains to H. polygyrus . CBA, C3H and A/J mice all tolerated heavy infections and are assessed as poor responders. In contrast, DBA/2, 129/J and BALB/c mice performed variably between experiments, some tolerating heavy worm burdens comparable to those in poor responders, and some showing evidence of resistance, although only in one experiment with female 129/J females and one with female BALB/c was the pattern and extent of worm loss much like that in SWR mice. Because the genetic relationships between six of the strains exploited in this study are now well-understood, our results should enable analysis through single nucleotide polymorphisms and thereby provide more insight into the role of the genes that control resistance to H. polygyrus. [ABSTRACT FROM AUTHOR]

Macrophages play an important role in the formation of granulomas and the clearance of Brugia pahangi infections in mice. However, the factors responsible for the recruitment of these cells to the site of infection are not known. In this study we examined the role of the C-C chemokine ligand 2 (CCL2; also known as macrophage chemotactic factor – MCP1) in macrophage recruitment in intraperitoneal infections with B. pahangi . We observed that CCL2 was expressed by peritoneal exudate cells and was present in the sera of wild-type mice. Serum levels of CCL2 peaked twice during the immune response, once during the early, acute phase and again during the late, chronic phase. To further elucidate the role of this chemokine in the anti-filarial immune response, we compared CCL2 deficient (CCL2−/– ) mice to wild-type mice. We observed that macrophage recruitment was impaired only during the acute phase in the former. While macrophage recruitment was unaffected during the chronic phase, increased accumulation of B and T lymphocytes was seen in these mice. We further report that larval clearance and the in vitro adhesion of PECs to larvae were unimpaired in these mice. [ABSTRACT FROM AUTHOR]