Kolaczkowska E, Seljelid R, Plytycz B
Department of Experimental Pathology, Institute of Medical Biology, University of Tromsø, Norway.
J Leukoc Biol. 2001 Jan;69(1):33-42.
Zymosan-induced peritonitis was investigated in mast cell-deficient WBB6F1 mice and in Balb/c mice pretreated with mast cell stabilizer (cromolyn) or antagonists of histamine receptors (mepyramine, triprolidine, cimetidine, or ranitidine). The inherited mast cell deficiency in W/Wv knockouts of WBB6F1 mice impaired significantly the level of histamine and plasma exudation (measured 30 min after stimulation) as well as the influx of exudatory leukocytes, accumulation of plasma and exudate chemoattractants, and the release of proinflammatory cytokines (TNF-alpha, IL-1beta, and IL-6) measured at 6 h of inflammation. All of those factors were fully restored after selective intraperitoneal reconstitution of W/Wv mice with bone marrow-derived mast cells from their control +/+ counterparts. Cromolyn pretreatment of Balb/c mice reduced exclusively the early plasma exudation and histamine influx. Blocking of histamine receptors inhibited not only the early plasma exudation but also temporarily diminished primary leukocyte influx and levels of MCP-1 and IL-1beta. In conclusion, mast cells play an important role in the initiation of zymosan-induced peritonitis and modulate its further course.
在肥大细胞缺陷的WBB6F1小鼠以及用肥大细胞稳定剂（色甘酸）或组胺受体拮抗剂（甲氧苄胺嘧啶、曲普利啶、西咪替丁或雷尼替丁）预处理的Balb/c小鼠中研究了酵母聚糖诱导的腹膜炎。WBB6F1小鼠W/Wv基因敲除导致的遗传性肥大细胞缺陷显著损害了组胺水平和血浆渗出（刺激后30分钟测量），以及渗出性白细胞的流入、血浆和渗出液趋化因子的积累，以及在炎症6小时时测量的促炎细胞因子（TNF-α、IL-1β和IL-6）的释放。在用来自对照+/+同窝小鼠的骨髓来源肥大细胞对W/Wv小鼠进行选择性腹腔重建后，所有这些因素都完全恢复。对Balb/c小鼠进行色甘酸预处理仅减少了早期血浆渗出和组胺流入。组胺受体阻断不仅抑制了早期血浆渗出，还暂时减少了初级白细胞流入以及MCP-1和IL-1β的水平。总之，肥大细胞在酵母聚糖诱导的腹膜炎的起始中起重要作用，并调节其后续进程。
