Brown A S, Davis J M, Murphy E A, Carmichael M D, Carson J A, Ghaffar A, Mayer E P
Division of Applied Physiology, Arnold School of Public Health, University of South Carolina, SC 29208, USA.
J Appl Physiol (1985). 2007 Nov;103(5):1592-7. doi: 10.1152/japplphysiol.00677.2007. Epub 2007 Sep 6.
Exhaustive exercise has been associated with an increased risk for upper respiratory tract infections in mice and humans. We have previously shown (Brown AS, Davis JM, Murphy AE, Carmichael MD, Ghaffer A, Mayer EP. Med Sci Sports Exerc 36: 1290-1295, 2004) that female mice are better protected from the lethal effects of herpes simplex virus type 1 (HSV-1) infection, both at rest and following exercise stress, but little is known about possible mechanisms. This study tested the effects of estrogen on HSV-1 infection and macrophage antiviral resistance following repeated exhaustive exercise. Female mice were assigned to either exercise (Ex) or control (C): intact female (I-C or I-Ex), ovariectomized female (O-C or O-Ex), or ovariectomized estrogen-supplemented female (E-C or E-Ex). Exercise consisted of treadmill running to volitional fatigue ( approximately 125 min) for 3 consecutive days. Intact female mice had a later time to death than O and E (P < 0.05) and fewer deaths than both O and E (P < 0.05). Exercise stress was associated with increased time to sickness (P < 0.05) and symptom severity at days 6 and 12-21 postinfection (P < 0.05) and decreased macrophage antiviral resistance (P < 0.001) in all groups. E had increased symptom severity at days 6 and 13-21 postinfection (P < 0.05). Results indicate that intact female mice are better protected from the lethal effects of HSV-1 infection and that exercise stress had a similar negative impact in all groups. This protective effect was lost in ovariectomized mice, but it was not reinstated by 17beta-estradiol replacement. This indicates that other ovarian factors, alone or in combination with estrogen, are responsible for the protective effects in females.
力竭运动与小鼠和人类上呼吸道感染风险增加有关。我们之前已经表明（Brown AS, Davis JM, Murphy AE, Carmichael MD, Ghaffer A, Mayer EP. 《医学与科学运动与锻炼》36: 1290 - 1295, 2004），雌性小鼠在休息和运动应激后，对1型单纯疱疹病毒（HSV - 1）感染的致死效应具有更好的保护作用，但对于可能的机制知之甚少。本研究测试了雌激素对反复力竭运动后HSV - 1感染和巨噬细胞抗病毒抗性的影响。将雌性小鼠分为运动组（Ex）或对照组（C）：完整雌性（I - C或I - Ex）、去卵巢雌性（O - C或O - Ex）或去卵巢补充雌激素雌性（E - C或E - Ex）。运动包括连续3天在跑步机上跑步至自愿疲劳（约125分钟）。完整雌性小鼠的死亡时间晚于去卵巢和补充雌激素组（P < 0.05），且死亡数量少于去卵巢和补充雌激素组（P < 0.05）。运动应激与所有组感染后发病时间延长（P < 0.05）、感染后第6天和第12 - 21天症状严重程度增加（P < 0.05）以及巨噬细胞抗病毒抗性降低（P < 0.001）相关。补充雌激素组在感染后第6天和第13 - 21天症状严重程度增加（P < 0.05）。结果表明，完整雌性小鼠对HSV - 1感染的致死效应具有更好的保护作用，并且运动应激在所有组中都有类似的负面影响。这种保护作用在去卵巢小鼠中丧失，但17β - 雌二醇替代并未恢复。这表明其他卵巢因素单独或与雌激素联合，对雌性具有保护作用。
