Cold stress-induced modulation of cell immunity during acute Toxoplasma gondii infection in mice
Cold stress-induced modulation of cell immunity during acute Toxoplasma gondii infection in mice
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DOI：
10.2307/3285776
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发表时间：
1999-06-01
影响因子：
1.3
通讯作者：
Monroy, FP
中科院分区：
文献类型：
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作者：
Banerjee, SK;Aviles, H;Monroy, FP
急性期弓形虫感染会导致小鼠和人免疫功能的非特异性抑制。本研究检查了物理应激源的影响，即，冷应激（CS）对小鼠T.弓形虫感染在我们的应激模式中，将雌性BALB/c小鼠置于冷水（1 +/-0.5 ℃）中，每天5分钟，持续8天。在用干扰素-γ/脂多糖（CS + ACT）体内活化CS和体外感染T.弓形虫速殖子CS + ACT小鼠的腹膜巨噬细胞显示与对照但激活的细胞（ACT）相比亚硝酸盐产生减少。用弓形虫感染BALB/c小鼠，观察其急性期脾细胞对伴刀豆球蛋白A（ConA）、抗CD_3抗体和弓形虫溶胞抗原（TLA）体外刺激的增殖反应。刚地。CS和感染（CS + INF）的小鼠在第8天和第15天脾细胞增殖最大，随后在接种后第28天（PI）下降。相比之下，感染的小鼠没有受到压力（INF）显示减少脾细胞增殖在第8和15天，随后在第28天PI增加。在急性感染期间，CS + INF组的死亡率低于INF组。这些结果提示CS可能改变了T.弓形虫感染通过调节急性期反应，引起宿主和寄生虫之间的暂时不平衡状态。
Infection with Toxoplasma gondii in the acute phase results in nonspecific suppression of immunologic function in mice and humans. The present study examined the effects of a physical stressor, i.e., cold stress (CS), on macrophage function (nitrite production, parasite survival) and splenic blastogenesis in the acute phase of murine T. gondii infection. In our stress paradigm, female BALB/c mice were placed in cold water(1 +/- 0.5 C), 5 min each day for 8 days. Nitrite production and parasite survival were measured in cultured peritoneal macrophages obtained from mice subjected to CS after in vivo activation with interferon-gamma/lipopolysaccharide (CS + ACT), and in vitro infection with T. gondii tachyzoites. Peritoneal macrophages from CS + ACT mice showed decreased nitrite production compared to control but activated cells (ACT). Spleen cell proliferation to in vitro stimulation with the mitogens concanavalin A (Con A) and anti-CD3, and Toxoplasma lysate antigen (TLA) was measured in splenocytes obtained from BALB/c mice during the acute phase of infection with T. gondii. Mice subjected to CS and infection (CS + INF) had maximum splenocyte proliferation on days 8 and 15 followed by a subsequent decline on day 28 postinoculation (PI). In contrast, infected mice not subjected to stress (INF) showed decreased splenocyte proliferation on days 8 and 15 followed by an increase on day 28 PI. The rate of mortality was decreased in the CS + INF compared to the INF group during acute infection. These results suggest that CS may alter the pathogenesis of T. gondii infection by modulating acute-phase responses, provoking a state of transient disequilibrium between the host and parasite.