Immune Response to a Trichinella spiralis infection in high-runner mice


Meeting Abstract

86.1  Friday, Jan. 7  Immune Response to a Trichinella spiralis infection in high-runner mice DLUGOSZ, EM*; SCHUTZ, H; MEEK, TH; ACOSTA, W; DOWNS, CJ; PLATZER, EG; CHAPPELL, MA; GARLAND, T Jr; Univ. of California, Riverside; Univ. of Nevada, Reno edlug001@ucr.edu

Mice bred for high voluntary wheel running (HR) have high baseline circulating corticosterone and increased daily energy expenditure as compared with non-selected Control (C) lines. High corticosterone may suppress immune function and competing energy demands may limit an individual’s ability to mount an immune response. We hypothesized that HR would have a reduced immune response and therefore decreased ability to fight an infection. Trichinella spiralis is an ecologically relevant nematode common in mammals. Infections have an acute, intestinal phase while the nematode is migrating, reproducing, and traveling throughout the bloodstream, followed by a chronic phase with larvae encysted in muscles. 50 adult males from generation 55 were infected with ~300 J1 T. spiralis larvae and 45 mice were sham-infected. Blood was collected throughout the infection cycle and leukocyte profiles as well as IgE levels were later quantified. During the chronic phase of infection, 6 days of wheel access were followed by 2 days of maximum aerobic performance (VO2max) trials. Infected HR mice had significantly lower IgE levels compared with infected C mice. However, we found no statistical difference between infected HR and C mice in numbers of encysted larvae within the diaphragm (a standard index of infection level). As expected, VO2max was significantly higher in HR mice and lower in infected mice, with no linetype X infection interaction. Results agree with previous studies suggesting that locomotor abilities are decreased during the chronic phase of infection. Contrary to our hypothesis, however, selective breeding for high voluntary wheel running does not appear to have had a substantial negative impact on immune function. NSF IOB-0543429 to TG.

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