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The purpose of this investigation was to determine the effects of different doses of exercise on the ability of Propionibacterium acnes (P. acnes) to induce major histocompatibility complex (MHC) II antigen expression on macrophages (M phi's). Pathogen-free male Balb/c mice were exercised on a treadmill moderately (MOD, 15-17 m/min, 5% grade, 30 min/day) or exhaustively (EXH, 15-40m/min, 5% grade, 2-4hr/day) for a period of 7 days during P. acnes-induced inflammation. A control group (CON) consisted of animals exposed to the treadmill environment and handling. Sub-optimal (0.03 mg/g b.wt., i.p.) and optimal (0.08 mg/g b.wt.) doses of P. acnes were used to increase M phi MHC II expression. Animals were sacrified on Day 7 and M phi's were harvested by peritoneal lavage. Direct immunofluorescent staining was performed by incubating peritoneal exudate cells (10[6]) with an FITC-labeled anti-mouse MHC II (I-A[d]) antibody. Basal expression of MHC II was not affected by exercise. There were no significant differences among the groups in the percentage of M phi's expressing MHC II at any dose of P. acnes. However, EXH significantly (p < 0.05) suppressed the expression (mean fluorescent intensity, MFI) of MHC II when compared to MOD (37.1+/-1.95 [mean+/-sem] vs 49.1+/-2.15, p < 0.05) at the suboptimal P. acnes dosage. At the optimal P. acnes dose, both MOD and EXH significantly suppressed (27+/-1.6, 25+/-2.2 and 41.5+/-3.2, for EXH, MOD, and CON, respectively, p<0.0001) P. acnes-induced M phi MHC II MFI. Plasma corticosterone was highly (r=-0.71, p = 0.001) inversely correlated with M phi MHC II expression. However, exercise failed to affect P. acnes-induced production of interferon-gamma. These data suggest that, dependent on the degree of stimulation, exercise can negatively affect M phi expression of MHC II, an effect that may be detrimental to the M phi's ability to present antigen to T lymphocytes.

We investigated the effects of a graded maximal exercise treadmill test on natural killer (NK) cell number, activity, and responsiveness to interferon-alpha (IFN-alpha) in young (22+/-0.7 yrs) and elderly (65+/-0.8 yrs) sedentary subjects. NK cell cytotoxicity (NKCC) was determined using Ficoll purified peripheral blood mononuclear cells (PBMCs) by a 51Cr release assay against NK-sensitive (K562) and NK-insensitive (Daudi) target cells at various effector:target (E:T) ratios before and immediately after exercise. PBMCs were incubated with rhu IFN-alpha (125 and 250u/10(6) PBMCs) or without for 2 hrs before addition to the 51Cr release assay. There were no differences in unstimulated NKCC against K562 or Daudi targets between the old and the young despite significantly (p=.01) higher percentages of CD56+ NK cells (21.1+/-2.3% in old vs 12.5+/-2.5% in young, pre-exercise). IFN-alpha increased NKCC versus both targets, and NK cells from old subjects were hyporesponsive to IFN-alpha stimulation; this was especially evident at low E:T ratios versus Daudi cells. Maximal exercise significantly increased (50-200%) unstimulated NKCC versus K562 and Daudi targets similarly in both young and old and increased the percentage of CD56+ cells in the PBMC fraction to 33.3+/-3.7% and 23.3+/-3.6% in old and young, respectively. We found a significant correlation between %CD56+ and basal NKCC versus K562s and Daudi cells in the young (i.e., r=.55; p=.02 vs K562s), but not the old (i.e., r=.20; p=.29 vs K562s) subjects. This indicates that, in the young, part of the exercise-induced increase in NKCC is due to an increase in NK cell number. Maximal exercise did not affect unstimulated per cell killing of K562s, but tended to increase per cell killing of Daudis. These results indicate that CD56+ cells from old subjects have an intrinsic defect in their ability to perform cytolysis and respond to IFN-alpha. Furthermore, a single bout of maximal exercise increases NKCC and CD56+ cell number similarly in both young and old subjects regardless of the target cell used.