Macrophage activation by culture in an anoxic environment.
Macrophage activation by culture in an anoxic environment.
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DOI：
10.4049/jimmunol.155.9.4391
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发表时间：
1995-11
影响因子：
4.4
通讯作者：
Jorge E. Albina;W. Henry;B. Mastrofrancesco;B. Martin;J. Reichner
中科院分区：
文献类型：
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作者：
Jorge E. Albina;W. Henry;B. Mastrofrancesco;B. Martin;J. Reichner
在巨噬细胞浸润高峰期间，大鼠实验伤口的细胞外氨基酸组成具有伤口液中存在的升高的精氨酸酶活性的印记：在该空间中发现L-精氨酸的浓度显著低于血浆中可检测到的浓度，而L-鸟氨酸的浓度显著高于血浆中可检测到的浓度。此时未发现L-瓜氨酸或NO2-蓄积形式的一氧化氮合酶（NOS）活性证据。然而，伤口衍生的巨噬细胞在培养物中通过精氨酸酶和NOS代谢L-精氨酸。鉴于NOS对O2的需求和伤口中O2张力的降低，进行实验以确定O2可用性对伤口衍生的巨噬细胞代谢L-精氨酸的作用。结果表明，除了抑制NOS外，在缺氧环境中培养伤口衍生的巨噬细胞提供了激活信号，显著增加总L-精氨酸代谢、精氨酸酶活性、NOS蛋白含量以及TNF-α和IL-6的释放。无论是居民，也不是棒状杆菌引起的腹腔巨噬细胞响应缺氧培养的L-精氨酸利用率，脱氢酶活性的增加，或在居民巨噬细胞的情况下，在NOS蛋白含量。缺氧诱导的伤口源性巨噬细胞中TNF-α和IL-6释放的增强也见于驻留的腹腔巨噬细胞中。因此，缺氧似乎是从不同部位获得的巨噬细胞激活相关性状的诱导物。
The extracellular amino acid composition of experimental wounds in rats during peak macrophage infiltration bears the imprint of the elevated arginase activity present in wound fluid: L-arginine is found in this space in concentrations markedly lower, and L-ornithine in concentrations markedly higher, than those that are detectable in plasma. No evidence, in the form of L-citrulline or NO2- accumulation, can be found at this time for nitric oxide synthase (NOS) activity. Wound-derived macrophages, however, metabolize L-arginine through both arginase and NOS in culture. Given the requirements of NOS for O2 and the reduced O2 tension in wounds, experiments were performed to determine the role of O2 availability on the metabolism of L-arginine by wound-derived macrophages. Results demonstrated that, beyond inhibiting NOS, culture of wound-derived macrophages in an anoxic environment provided an activation signal, markedly increasing total L-arginine metabolism, arginase activity, NOS protein content, and the release of TNF-alpha and IL-6. Neither resident nor Corynebacterium parvum-elicited peritoneal macrophages responded to anoxic culture with increases in L-arginine utilization, arginase activity or, in the case of resident macrophages, in NOS protein content. The enhanced TNF-alpha and IL-6 release induced by anoxia in wound-derived macrophages was also found in resident peritoneal macrophages. Anoxia appears to act, then, as an inducer of activation-associated traits in macrophages obtained from different sites.