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The ability of Mycobacterium bovis Bacille Calmette-GuÃ©rin (BCG) to induce a state of heightened resistance to subsequent lethal infection with virulent Mycobacterium tuberculosis H37Rv has been attributed to its ability to induce T cell-mediated innate and adaptive immune responses. Here, we show that before intraperitoneal infection with a low virulence strain of M. tuberculosis, BCG enhanced the functional capacity of antigen-specific CD4(+) T cells in vivo. CD4(+) T cells isolated from mice immunized and then infected 5 days later exhibited a 5- to 6-fold increase in proliferation to M. tuberculosis antigen in vitro when compared with cells isolated from animals immunized with BCG alone. We also show that, after BCG immunization, IFN-gamma production by CD4(+) T cells was increased following restimulation with M. tuberculosis antigen, and that, while mice treated with BCG did not exhibit increased numbers of IFN-gamma-producing cells, IFN-gamma production per cell was enhanced in M. tuberculosis-stimulated BCG-immunized animals. Thus, BCG induced priming of Ag-specific CD4(+) T cells, which was reflected by enhanced antigen-specific T cell cytokine production and survival in vivo. These results suggest a potential mechanism by which BCG-primed T cells might contribute to enhanced resistance to acute infection during a tuberculosis epidemic.Imbalance between skeletal muscle mitochondrial function and efficiency in healthy trained men.
The main aims of the present study were to quantify skeletal muscle oxidative capacity in healthy trained men and to determine the relationship between exercise training and mitochondrial function. Thirteen healthy trained men performed constant-load bicycle exercise to determine their oxidative capacity. The exercise session consisted of a 90-s maximal cycle at 100 W, followed by 75 min of cycling at 75 W. Cytochrome c oxidase activity and citrate synthase (CS) activity were determined in order to determine mitochondrial density and CS activity in the plantar flexors. Exercise training did not influence mitochondrial density or CS activity. However, both maximal oxidative capacity, measured at the end of the exercise test (308 ± 69
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