Geudens N, Vanaudenaerde B M, Neyrinck A P, Van De Wauwer C, Vos R, Verleden G M, Verbeken E, Lerut T, Van Raemdonck D E M
Department of Laboratory of Experimental Thoracic Surgery, Katholieke Universiteit Leuven, 3000 Leuven, Belgium.
Transplant Proc. 2007 Oct;39(8):2659-62. doi: 10.1016/j.transproceed.2007.08.001.
In a murine model of lung ischemia-reperfusion injury (IRI), we previously demonstrated that lymphocytes increase in the alveolar space during the ischemic period. We hypothesized that these lymphocytes play an important role during ischemia in the development of lung IRI. In the present study, severe combined immunodeficiency (SCID) mice, lacking T cells, were used to further investigate our hypothesis. SCID and control mice underwent 90 minutes of left lung ischemia followed by 4 hours of reperfusion. A significant decrease in neutrophils, together with lower levels of interleukin-1beta, was found in SCID mice after reperfusion. We concluded that lymphocytes invading the lung during ischemia trigger an inflammatory response upon reperfusion. Antilymphocyte therapies in the donor should be further investigated as treatment strategies against IRI.
在小鼠肺缺血再灌注损伤（IRI）模型中，我们之前证明在缺血期肺泡间隙中的淋巴细胞会增加。我们推测这些淋巴细胞在肺IRI发生过程中的缺血期发挥重要作用。在本研究中，使用缺乏T细胞的严重联合免疫缺陷（SCID）小鼠来进一步研究我们的假设。SCID小鼠和对照小鼠经历了90分钟的左肺缺血，随后再灌注4小时。再灌注后，SCID小鼠的中性粒细胞显著减少，同时白细胞介素-1β水平降低。我们得出结论，缺血期间侵入肺的淋巴细胞在再灌注时引发炎症反应。作为针对IRI的治疗策略，应进一步研究供体中的抗淋巴细胞疗法。
