Ottonello Luciano, Ghio Massimo, Contini Paola, Bertolotto Maria, Bianchi Giordano, Montecucco Fabrizio, Colonna Marco, Mazzei Clemente, Dallegri Franco, Indiveri Franco
Divisions of Internal Medicine and Clinical Immunology, Department of Internal Medicine, University of Genoa Medical School, Viale Benedetto XV 6, I-16132 Genoa, Italy.
Transfusion. 2007 Aug;47(8):1395-404. doi: 10.1111/j.1537-2995.2007.01268.x.
Red blood cell (RBC) transfusion has been linked to increased susceptibility to infections in critically ill patients and to augmented incidence of postoperative infections. The mechanisms by which transfusions can induce immunosuppression are only partially defined. Recently, it has been demonstrated that RBC supernatants inhibit neutrophil migration. Such inhibitory activity is due to transforming growth factor (TGF)-beta1 contained in the supernatants that desensitize neutrophils to subsequent chemotaxic stimulation.
In ancillary experiments, it was observed that plasma from transfused patients maintained its capacity of inhibiting neutrophil chemotaxis several days after RBC transfusion. Thus, this study was planned to investigate the mechanism(s) responsible for the prolonged inhibition of neutrophil chemotaxis observed after RBC transfusion.
Plasma samples obtained from subjects who underwent RBC transfusion display a capability of inhibiting neutrophil chemotaxis, which is detectable up to 15 days after the transfusion. The inhibition is related to the capacity of FasL and HLA-I molecules contained in RBC supernatants to induce in vivo TGF-beta1 synthesis by neutrophils. The induction of TGF-beta1 secretion in neutrophils by HLA-I molecules depends on immunoglobulinlike transcript 1/CD85 triggering.
The property of RBC transfusion of inducing a sustained inhibition of neutrophil chemotaxis seems to be a potential mechanism that concurs to the susceptibility to infections in patients who receive transfusions. Furthermore, our findings, showing neutrophil production of TGF-beta1 in response to FasL and HLA-I molecules, confirm that neutrophils are endowed not only with effector functions but also with immunomodulatory properties possibly involved in the regulation of inflammatory processes.
红细胞（RBC）输血与重症患者感染易感性增加以及术后感染发生率升高有关。输血诱导免疫抑制的机制仅部分明确。最近，已证明红细胞上清液可抑制中性粒细胞迁移。这种抑制活性归因于上清液中所含的转化生长因子（TGF）-β1，它使中性粒细胞对随后的趋化刺激脱敏。
在辅助实验中，观察到输血患者的血浆在红细胞输血后数天仍保持其抑制中性粒细胞趋化性的能力。因此，本研究旨在探讨红细胞输血后观察到的中性粒细胞趋化性长期抑制的机制。
从接受红细胞输血的受试者获得的血浆样本显示出抑制中性粒细胞趋化性的能力，输血后长达15天均可检测到。这种抑制与红细胞上清液中所含的FasL和HLA-I分子诱导中性粒细胞在体内合成TGF-β1的能力有关。HLA-I分子诱导中性粒细胞分泌TGF-β1取决于免疫球蛋白样转录物1/CD85触发。
红细胞输血诱导中性粒细胞趋化性持续抑制的特性似乎是导致接受输血患者感染易感性增加的潜在机制。此外，我们的研究结果表明中性粒细胞对FasL和HLA-I分子产生TGF-β1，证实中性粒细胞不仅具有效应功能，还具有可能参与炎症过程调节的免疫调节特性。
