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Voluntary Wheel Running and Response to Vaccinia Virus Infection and Inoculation in Mice

766 May 31 3

30 PM - 3

45 PM

Pence, Brandt D.1; Ryerson, Melissa R.2; Bravo-Cruz, Ariana G.2; Woods, Jeffrey A. FACSM2; Shisler, Joanna L.2

Medicine & Science in Sports & Exercise: May 2017 - Volume 49 - Issue 5S - p 196–197
doi: 10.1249/01.mss.0000517376.41290.eb
B-44 Free Communication/Slide - Immunology Wednesday, May 31, 2017, 3: 15 PM - 4: 45 PM Room: 104

1University of Memphis, Memphis, TN. 2University of Illinois Urbana-Champaign, Urbana, IL.


(No relationships reported)

PURPOSE: Exercise has been shown to improve immune responses to viral infections and vaccines in several mouse models. However, previous pathogen studies have primarily used infections limited to the respiratory tract. Additionally, previous studies have utilized forced treadmill exercise paradigms, and voluntary wheel running (VWR) has been shown to have differential effects on the immune system in non-infection models. We examined whether VWR could improve morbidity and mortality to a 50% lethal dose of vaccinia virus (VACV), a systemic pathogen commonly used to examine immune responses. Additionally, we examined whether VWR could improve antibody response to a replication-deficient strain of VACV, mimicking a vaccination.

METHODS: Male C57Bl/6 J mice underwent 8 weeks of VWR or remained sedentary, then were infected intranasally with 10^5 PFU VACV strain WR. Mice were followed 14 days for mortality, and body weights and food intakes were recorded daily. In a similar manner, mice in the vaccination study ran or were sedentary for 8 weeks, then were given 10^6 PFU of replication-deficient VACV strain MVA intraperitoneally. Blood was collected under anesthesia from the retro-orbital sinus prior to MVA inoculation and at 1, 2, and 4 weeks post-inoculation, and anti-VACV IgG titer was determined by enzyme-linked immunosorbant assay.

RESULTS: VWR did not improve mortality due to VACV infection (p=0.26), although fewer VWR mice (4/10) died compared to sedentary (SED, 6/10). VWR did not prevent body weight loss due to infection compared to SED (p = 0.20), although VWR mice loss slightly less weight (4%) compared to SED through the first 6 days post-infection. Food intake, the reduction of which is a marker of sickness behavior, was significantly reduced in SED post-infection compared to VWR (p=0.05). In the vaccination experiment, VWR mice developed a greater IgG antibody response, although this was not significant (p=0.22).

CONCLUSIONS: VWR did not protect against mortality to VACV or prevent infection-induced weight loss, and VWR did not enhance antibody responses. However, there were non-significant trends towards VWR-related improvements in these outcomes, and post-infection food intake was improved by VWR. Funded by ACSM Research Endowment Grant to BDP.

© 2017 American College of Sports Medicine