Elevation of serum chemotactic factor inactivator activity during acute inflammatory reactions in patients with hypersensitivity pneumonitis.
Elevation of serum chemotactic factor inactivator activity during acute inflammatory reactions in patients with hypersensitivity pneumonitis.
复制标题
过敏性肺炎患者急性炎症反应期间血清趋化因子灭活剂活性升高。
DOI：
10.1164/arrd.1982.125.5.612
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Fink,JN
中科院分区：
文献类型：
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作者：
Kreutzer,DL;McCormick,JR;Thrall,RS;Hupp,JR;Moore,VL;Fink,JN
炎症介质，如源自补体系统激活的血管活性因子和趋化因子，是非常有效的生物多肽，受到特定血清衍生调节剂的严格控制，例如，过敏毒素灭活剂（AI）和趋化因子灭活剂（CFI）。我们之前已经证明，血清趋化因子失活剂浓度在慢性炎症状态下发生改变；在这里，我们证明血清CFI活性的快速升高发生在急性炎症反应的患者患有过敏性肺炎。具体来说，用2毫升无菌鸽子血清进行气溶胶攻击后，对超敏性肺炎（鸽子饲养者病）患者和对照组（无症状）的血清CFI浓度进行了评估。在攻毒后4小时，超敏性肺炎患者血清CFI浓度迅速上升至攻毒前血清浓度的3倍。无症状（对照）受试者暴露于鸽子血清后血清CFI浓度没有增加。在独立研究中，我们也证明了(1)糖原性腹膜炎的兔，(2)静脉输注c5衍生趋化因子的兔，以及(3)进行血液透析的患者血清CFI浓度升高。这些综合数据清楚地表明，在患者和动物群体中，血清CFI活性在急性炎症反应期间迅速升高，并提示血清CFI可能代表炎症期间升高的“超急性”相反应物。CFI的升高可能是由炎症过程中产生的炎症介质引起的。因此，急性炎症期间血清CFI浓度的急性升高可能代表控制系统在炎症反应期间对机体的调节需求作出反应。
Inflammatory mediators such as the vasoactive and chemotactic factors derived from the activation of the complement system are extremely potent biological peptides that are under rigid control of specific serum-derived regulators, eg, the anaphylatoxin inactivator (AI) and the chemotactic factor inactivator (CFI). We have previously demonstrated that serum chemotactic factor inactivator concentrations are altered during chronic inflammatory states; here we demonstrate that a rapid elevation of serum CFI activity occurs during acute inflammatory reactions in patients suffering from hypersensitivity pneumonitis. Specifically, serum CFI concentrations were evaluated in patients with hypersensitivity pneumonitis (pigeon breeder's disease) and control subjects (asymptomatic) after aerosol challenge with 2 ml of sterile pigeon serum. At 4 h postchallenge, serum CFI concentrations in the patients with hypersensitivity pneumonitis increased rapidly to 3 times the prechallenge serum concentrations. Asymptomatic (control) subjects showed no increase in serum CFI concentrations after exposure to pigeon serum. In independent studies, we have also demonstrated that serum CFI concentrations are elevated in (1) rabbits with glycogen-induced peritonitis,(2) rabbits after intravenous infusion of C5-derived chemotactic factors, and (3) patients undergoing hemodialysis. These combined data clearly demonstrate that serum CFI activity is rapidly elevated during acute inflammatory reactions within both patient and animal populations, and suggest that serum CFI may represent a" hyperacute" phase reactant that is elevated during inflammation. Possibly, this elevation of CFI may be induced in response to inflammatory mediators produced during inflammation. Thus, the acute elevation of serum CFI concentrations that occurs during acute inflammation may represent the control system that would be responsive to the regulatory needs of the body during inflammatory reactions.