Garssen J, van Loveren H, van der Vliet H, Nijkamp F P
University of Utrecht, Faculty of Pharmacy, Department of Pharmacology, The Netherlands.
Br J Clin Pharmacol. 1990;30 Suppl 1(Suppl 1):153S-155S. doi: 10.1111/j.1365-2125.1990.tb05491.x.
Inadequate reactions of the immune system, i.e. allergic or hypersensitivity reactions, can lead to lung tissue injury. We investigated the relationship of type IV hypersensitivity, as an example of IgE independent hypersensitivity, with the induction of airway hyperreactivity. After antigen challenge (picrylsulphonic acid (PSA] in picrylchloride (PCl) sensitized mice, peribronchial and perivascular accumulation of mononuclear cells was found that was maximal 48 h after challenge. At several time points after challenge, changes in smooth muscle tone of mouse isolated tracheas were measured isometrically. In sensitized mice the response to carbachol was increased, reaching a maximum 48 h after challenge. This hyperreactivity was not found in athymic (nude) mice. We concluded from these data that airway hyperreactivity can be immunologically induced other than by IgE.
免疫系统反应不足,即过敏或超敏反应,可导致肺组织损伤。我们以IV型超敏反应为例,研究了IgE非依赖性超敏反应与气道高反应性诱导之间的关系。在用苦味酸氯(PCl)致敏的小鼠中,用苦味磺酸(PSA)进行抗原攻击后,发现支气管周围和血管周围有单核细胞积聚,在攻击后48小时达到最大值。在攻击后的几个时间点,等长测量小鼠离体气管平滑肌张力的变化。在致敏小鼠中,对卡巴胆碱的反应增强,在攻击后48小时达到最大值。在无胸腺(裸)小鼠中未发现这种高反应性。我们从这些数据得出结论,气道高反应性可通过免疫诱导而非IgE诱导产生。