Abstract

Voluntary wheel running exercise induced higher antigen-specific IgG in circulating blood is well recognized in mice. This antibody response may be regulated by an exercise-induced mechanism that protects against IgG catabolism. The recent hypothesis that the β2-microglobulin gene is implicated in IgG protection is investigated further on mice voluntary wheel running. Male C57BL/6N mice were intraperitoneally immunized with 0.375 μg/kg (body weight) of tetanus toxoid to induce primary and secondary antibody responses. At the peak concentration of blood tetanus toxoid specific IgG in this experiment, we administered 125I-labeled mouse IgG. To determine how 125I–IgG half-life is prolonged in voluntary wheel running exercised mice, we observed the tissue radioactivity 125I–IgG. Significantly higher blood IgG concentrations were demonstrated in the exercised group compared to non-exercised group ( P < .05). The mean value of radioactivity in the liver was higher in the exercised group ( P < .05). Furthermore, extracted IgG concentration of exercised mouse liver was higher than that of non-exercised group ( P < .05). Immunohistochemical analysis showed dramatically increased tissue IgG in the liver of the exercised group ( P < .05). The gene expression of β2-microglobulin was up-regulated in the exercised mouse liver ( P < .05). There is a significant correlation between liver accumulation of 125I–IgG and 125I–IgG concentration in the blood ( P < .05). In addition, there is a significant correlation between extracted total hepatic IgG and β2-microglobulin in the liver ( P < .05). These findings indicate that voluntary wheel running exercise-induced liver β2-microglobulin expression is related to lower IgG clearance in the blood.

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