Abstract

Helminthologically naive merino sheep were given either a single infection of 30,000 or a trickle infection of 6000 Trichostrongylus colubriformis infective larvae (TcL3) per week. Faecal egg counts started to fall after 8 weeks in the single infection and after 11 weeks in the trickle infection. Small intestinal contents were collected from indwelling intestinal fistulae over the next 14 weeks. Concentrations of sheep mast cell protease (SMCP) in these contents increased to highest levels 9–11 weeks and 6–10 weeks after the single infection and from the start of the trickle infection, respectively. Similarly, peptidyl leukotriene (PLT) concentrations were highest at 6 weeks and at 6–9 and 13 weeks, respectively. Histamine concentrations increased slightly after both infections to peak values at 7 weeks and 9 weeks, respectively. Inhibition of migration of larvae in vitro was increased in contents sampled at 8 weeks after the single infection and after 6–10 weeks of the trickle infection. Another 2 groups of sheep were immunised by repeated infections with TcL3. Gut contents from 1 group sampled immediately before and after challenge with 30,000 TcL3 at 0 and 18 days had increased levels of larval migration inhibitory (LMI) activity throughout the 35 day period, especially 7–14 days after challenge (DAC). The mediators SMCP increased significantly 5–7 DAC while PLT increased 7–14 DAC. In the second group of immunised sheep, levels of SMCP and PLT increased rapidly within 1 DAC and further increased 3–14 DAC. Increased concentrations of platelet activating factor PAF occurred only at 14 DAC, while LMI activity was greatest in mucus collected 5–8 DAC. Since increased concentrations of these mediators occurred around the time when egg counts started to decline in primary infections and were increased after challenge of immune sheep, the results suggest roles for the mediators and/or their cellular source in the expression of immunity.

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