Carrageenan-induced acute inflammation in the mouse air pouch synovial model. Role of tumour necrosis factor

Carrageenan-induced acute inflammation in the mouse air pouch synovial model. Role of tumour necrosis factor
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DOI:
10.1080/09629359791901
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发表时间:
1997-02-01
影响因子:
4.6
通讯作者:
Ghezzi, P
Ghezzi, P
中科院分区:
医学3区
文献类型:
--
作者:
Romano, M;Faggioni, R;Ghezzi, P

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采用小鼠气囊炎症模型,研究细胞因子、前列腺素E(2)(PGE(2))在角叉菜胶致急性局部炎症不同阶段与细胞迁移的相互作用。血清中白介素1(IL-1)、白介素6(IL-6)、肿瘤坏死因子(TNF)、血清胺-A(SAA)和Fe++水平与对照组无明显差异,提示局部未见全身炎症改变,渗出液体积和囊中白细胞数逐渐增加,直至7d。前列腺素E(2)的生产也是如此。未检测到IL-1,但IL-6和肿瘤坏死因子在治疗后5~24小时达到高峰,随后迅速下降,抗肿瘤坏死因子抗体在治疗后24小时对细胞迁移抑制达50%。白介素10(IL-10)可几乎完全抑制肿瘤坏死因子的产生,使细胞迁移减少60%。角叉菜胶诱导的炎症反应受抗炎药物的调节。地塞米松(DEX)或吲哚美辛(INDO)可抑制细胞迁移,降低渗出液中的肿瘤坏死因子浓度。前列腺素E(2)的产生或血管通透性与袋中细胞的数量无关。局部肿瘤坏死因子似乎在这个模型中扮演着重要的角色,尤其是在炎症过程的第一阶段,对于白细胞的迁移。总而言之,气囊似乎是研究局部炎症早期事件,特别是细胞因子和细胞迁移作用的一个很好的模型。
WE used the mouse air pouch model of inflammation to study the interaction between cytokines, prostaglandin E(2) (PGE(2)) and cell migration during the various phases of acute local inflammation induced by carrageenan. In serum, the levels of interleukin 1 (IL-1), interleukin 6 (IL-6), tumour necrosis factor (TNF), serum amiloid-A (SAA) and Fe++ were never different from controls, indicating that no systemic inflammatory changes were induced Locally the exudate volume and the number of leukocytes recruited into the pouch increased progressively until 7 days after carrageenan. The same was true for PGE(2) production. We could not measure IL-1 but the production of IL-6 and TNF reached a maximum after 5-24 h then quickly decreased Anti-TNF antibodies inhibited cell migration by 50% 24 h after treatment. Pretreatment with interleukin 10 (IL-10) inhibited TNF production almost completely and cell migration by 60%. Carrageenan-induced inflammation was modulated by anti-inflammatory drugs. Pretreatment with dexamethasone (DEX) or indomethacin (INDO) inhibited cell migration and reduced the concentration of TNF in the exudate. Production of PGE(2) or vascular permeability did not correlate with the number of cells in the pouch. Local TNF seems to play an important role in this model, particularly for leukocyte migration in the first phase of the inflammatory process. In conclusion, the air pouch seems to be a good model for studying the regulation of the early events of local inflammation, particularly the role of cytokines and cell migration.