IL-33参与烧冲复合伤人与小鼠肺损伤机制的研究
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摘要
目的：烧冲复合伤是军事冲突、恐怖袭击、交通事故等突发事件中最常见的损伤类型之一。烧冲复合伤后肺脏损伤导致即时死亡的发生率高达47%。急性肺损伤(ALI)和急性呼吸窘迫综合症(ARDS)是烧冲复合伤早期死亡的主要原因之一,烧冲复合伤后即刻引起低血容量性休克与炎症级联反应。大量研究结果显示在ALI/ARDS的发病过程中,细胞因子与中性粒细胞发挥了关键性的作用。IL-33是新近发现的一种细胞因子,属于IL-1家族。IL-33mRNA表达于人类与小鼠的多个器官和不同类型的细胞,在蛋白水平,IL-33主要表达在上皮细胞、内皮细胞和纤维细胞。IL-33能够促进中性粒细胞趋化至感染部位减轻脓毒症。然而,在烧冲复合伤后肺组织IL-33与中性粒细胞是否存在这种机制仍不清楚。因此,我们建立重度烧冲复合伤动物模型,探讨在烧冲复合伤动物模型与烧冲复合伤患者中IL-33是否参与肺损伤。
方法：利用野生型C57BL/6小鼠与IL-33转基因小鼠分别建立烧冲复合伤、冲击伤、烧伤动物模型,小鼠随机分为正常对照组,烧伤组,冲击伤组,烧冲复合伤组。通过免疫组织化学法分别检测肺组织髓过氧化物酶(myeloperoxidase,MPO)、白介素-33(IL-33)、G蛋白偶联受体-2(GRK2)、趋化因子CXCR2的表达。透射电镜(transmission electron microscopy)观察肺组织超微结构的变化。real-time RT-PCR检测IL-33mRNA与GRK2mRNA的表达。酶联免疫吸附实验(ELISA)检测血浆IL-6与TNF-a浓度。Micro-CT观察肺组织的变化。同时,通过免疫组织化学法检测烧冲复合伤患者伤后24小时肺组织MPO、IL-33的表达。酶联免疫吸附实验检测烧冲复合伤患者血浆IL-6与TNF-a浓度。胸部X-ray观察肺组织的变化。
结果：
1.我们以5g8701炸药为爆炸源,距离爆炸源43cm,53cm,63cm分别建立冲击伤动物模型,压力值分别为200Kpa,94Kpa,88.3Kpa,根据冲击伤诊断标准确定中度冲击伤距离为53cm。
2.我们的动物模型表明烧冲复合伤后肺组织严重损伤。与正常对照组小鼠肺组织肉眼观相比,烧伤组小鼠肺组织轻度充血；冲击伤组小鼠肺组织中度充血,可见约3处点灶状出血；复合伤组小鼠肺组织明显充血,可见约5处斑点状出血；烧冲复合伤组小鼠伤后24小时与正常对照组、烧伤组、冲击伤组相比,肺组织湿干比重、出血面积明显增大。
3.与各实验组相比,在致伤后24小时烧冲复合伤小鼠的呼吸频率(Rr)、潮气量(Tv)、每分通气量(Mv)、最大呼气流量(PEF)明显降低降低,然而呼气时间(Te)与吸气时间(Ti)显著延长。
4.伤后24小时micro-CT检查显示：正常对照组与烧伤组小鼠肺组织未见病变；冲击伤组小鼠左侧肺组织可见轻度的毛玻璃样变区域；烧冲复合伤组小鼠左侧肺组织可见中度毛玻璃样变区域。
5.烧冲复合伤野生型C57BL/6小鼠伤后24小时肺组织髓过氧化物酶(MPO)、白介素一33(IL-33)、G-蛋白偶联受体-2(GRK2)表达明显增强。与烧冲复合伤后IL-33转基因小鼠伤后24小时相比,烧冲复合伤野生型C57BL/6小鼠趋化因子(CXCR2)明显减少；与各实验组相比,烧冲复合伤组小鼠血浆IL-6与TNF-α浓度均明显升高。
6.在烧伤、冲击伤、烧冲复合伤小鼠肺组织中IL-33的阳性细胞数与GRK2阳性细胞数、MPO阳性细胞数均有显著的正相关(r=0.65,p=0.042；r=0.638, p=0.0047；r=0.764,p=0.001)(r=0.716,p=0.02；r=0.661,p=0.0037；r=0.755, p=0.012),与Mv呈负相关(r=-0.677,p=0.031;r=-0.68,p=0.03;r=-0.816,p=0.004).
7.烧冲复合伤尸检见伤侧肺组织表面可见散在的斑片状出血,HE染色观察见大面积肺泡内出血。肺组织标本免疫组化染色见IL-33阳性细胞数高表达区域MPO阳性细胞数也高表达。
8.烧冲复合伤患者伤侧肺组织呈中度毛玻璃样变。
结论：
1.成功的建立了一种烧冲复合伤小鼠动物模型,具体参数为：野生型C57BL/6小鼠距离爆炸源53cm,压力峰值94Kpa致中度冲击伤,即刻将中度冲击伤小鼠背部脱毛区置入90℃沸水中持续9s,造成小鼠背部25%TBSAⅢ度烫伤。
2. IL-33通过激活GRK2通路阻断趋化因子CXCR2下调促进中性粒细胞迁移参与烧冲复合伤小鼠肺损伤。
3.高表达的IL-33参与烧冲复合伤患者肺损伤。
Objective:Burn-blast combined injury is one of the most common injuries in military conflict, terrorist attacks, traffic accidents, and other emergencies. Lung injury after burn-blast combined injury results in immediate death in up to47%of cases. Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are the main reasons for abrupt death in such injuries. Hypovolemic shock develops immediately after such injuries, initiating the generalized inflammatory cascade. Prior research in ALI and ARDS has demonstrated the importance of cytokines and neutrophils. Therefore, we focused on investigating cytokine-mediated neutrophils in the lungs after burn-blast combined injury. IL-33is a recently described member of the IL-1family, which also includes IL-1α/β, IL-1Ra, and IL-18. IL-33mRNA is expressed by multiple organs and cell types in humans and mice. IL-33protein is mainly expressed by epithelial cells, endothelial cells, and fibroblasts. IL-33attenuates sepsis by enhancing neutrophil influx to the site of infection. However, the function of IL-33-enhanced neutrophil influx in lung injury is unclear, specifically after burn-blast combined injury. Therefore, we established a burn-blast combined injury mice model. We investigated that IL-33would promote the participation of neutrophil migration in lung injury.
Methods:Burn-blast combined injury was induced in wild-type (WT) mice and IL-33transgenic mice. Mice were randomly divided into control group, burn group, blast group and burn-blast combined group. Immunohistochemistry assay was used to detect myeloperoxidase (MPO), IL-33, GRK2and CXCR2in lung after burn-blast combined group. Transmission electron microscopy (TEM) was used for observation of changes in lung. Plasma IL-6and TNF-a levels were measured by ELISA kits. Micro-CT was used for observation of changes in lung. In addition, Immunohistochemistry assay was used to detect myeloperoxidase (MPO) and IL-33in humans with burn-blast combined (BBLP). Chest radiograph scans was used to detect lung in humans with burn-blast combined.
Results:
1.We found that the mice at a distance of53cm, which exposed to94Ka peak overpressure, was the moderate blast injury distance when compared to mice at a distance of43cm and63cm, in these distances they were exposed200Ka and88.3Ka peak-overpressure, respectively.
2. The lungs of mice in burn-blast combined group (BBL) were severely congestive and most mice had more than5hemorrhage spots. However, the lungs of mice in burn (BU) or blast group (BL) showed less degree of congestion. In addition, the lungs of mice in control group (CO) were normal. The burn-blast combined injury group showed a significantly greater wet-to-dry weight ratio than the blast group and burn groups. The lung hemorrhage area in the burn-blast combined injury group was significantly higher than that for the blast injury and burn groups.
3. Burn-blast combined injury mice showed concomitantly reduced respiratory rate (Rr), tidal volume (Tv), minute ventilation volume (Mv), peak expiratory flow (PEF) as compared to burn injured mice, blast injured mice, and control mice at24hours. However, after burn-blast combined injury, WT mice exhibited significant lengthening of expiratory time (Te) and inspiratory time (Ti) as compared to each experimental group of WT mice at24hours.
4. We found moderate ground-glass shadows were seen in the left lung tissue in the burn-blast combined injury group on performing micro-CT. However, ground glass slightly appeared in various regions of left lung in the blast group and no lesions in the lung tissue of the control group and burn group.
5. MPO-, IL-33-and GRK2-positive cells significantly increased in the lung after burn-blast combined injury. However, the number of CXCR2-positive cells in WT mice was lower than those in the lungs of IL-33transgenic mice after burn-blast combined injury; Burn-blast combined injury mice had elevated plasma concentrations of IL-6and TNF-α.
6. In burn-blast combined injured IL-33transgenic mice, blast-injured IL-33transgenic mice, and burn-injured IL-33transgenic mice., some significant positive correlations were observed between IL-33-positive cells and both GRK2-positive cells (r=0.65, p=0.042; r=0.638, p=0.0047; r=0.764, p=0.001, respectively) and MPO-positive cells (r=0.716, p=0.02; r=0.661, p=0.0037; r=0.755, p= 0.012, respectively). The correlation coefficients suggested a strong association between IL-33-positive and Mv in burn-injured mice (r=-0.677, p=0.031), blast-injured mice (r=-0.68, p=0.03), and burn-blast combined injury mice(r=-0.816, p=0.004).
7. A large area of alveolar hemorrhage was seen in the patient with burn-blast combined injury. Interestingly, an increased number of MPO cells accumulated in the same area that IL-33is typically expressed.
8. Lung chest radiograph scans of the patient with burn-blast combined injury showed moderate ground-glass shadows in the left lung, while other areas appeared normal or nearly normal.
Conclusions:
1. We successfully established a stable mice model with burn-blast combined injury, which is inflicted with moderate blast injury by placing C57BL/6mice53cm away from explosive source, generating pressure peak of94Kpa, followed by induction of25%TBSA full-thickness burns on the back with90℃water for9s.
2. Our results suggest IL-33increases neutrophil influx to the site of infection and inflammation through GRK2pathway to block the downregulation of CXCR2with burn-blast combined injury.
3. Our results suggest that increased IL-33is involved in lung injury in humans with burn-blast combined injury.
方法：利用野生型C57BL/6小鼠与IL-33转基因小鼠分别建立烧冲复合伤、冲击伤、烧伤动物模型,小鼠随机分为正常对照组,烧伤组,冲击伤组,烧冲复合伤组。通过免疫组织化学法分别检测肺组织髓过氧化物酶(myeloperoxidase,MPO)、白介素-33(IL-33)、G蛋白偶联受体-2(GRK2)、趋化因子CXCR2的表达。透射电镜(transmission electron microscopy)观察肺组织超微结构的变化。real-time RT-PCR检测IL-33mRNA与GRK2mRNA的表达。酶联免疫吸附实验(ELISA)检测血浆IL-6与TNF-a浓度。Micro-CT观察肺组织的变化。同时,通过免疫组织化学法检测烧冲复合伤患者伤后24小时肺组织MPO、IL-33的表达。酶联免疫吸附实验检测烧冲复合伤患者血浆IL-6与TNF-a浓度。胸部X-ray观察肺组织的变化。
结果：
1.我们以5g8701炸药为爆炸源,距离爆炸源43cm,53cm,63cm分别建立冲击伤动物模型,压力值分别为200Kpa,94Kpa,88.3Kpa,根据冲击伤诊断标准确定中度冲击伤距离为53cm。
2.我们的动物模型表明烧冲复合伤后肺组织严重损伤。与正常对照组小鼠肺组织肉眼观相比,烧伤组小鼠肺组织轻度充血；冲击伤组小鼠肺组织中度充血,可见约3处点灶状出血；复合伤组小鼠肺组织明显充血,可见约5处斑点状出血；烧冲复合伤组小鼠伤后24小时与正常对照组、烧伤组、冲击伤组相比,肺组织湿干比重、出血面积明显增大。
3.与各实验组相比,在致伤后24小时烧冲复合伤小鼠的呼吸频率(Rr)、潮气量(Tv)、每分通气量(Mv)、最大呼气流量(PEF)明显降低降低,然而呼气时间(Te)与吸气时间(Ti)显著延长。
4.伤后24小时micro-CT检查显示：正常对照组与烧伤组小鼠肺组织未见病变；冲击伤组小鼠左侧肺组织可见轻度的毛玻璃样变区域；烧冲复合伤组小鼠左侧肺组织可见中度毛玻璃样变区域。
5.烧冲复合伤野生型C57BL/6小鼠伤后24小时肺组织髓过氧化物酶(MPO)、白介素一33(IL-33)、G-蛋白偶联受体-2(GRK2)表达明显增强。与烧冲复合伤后IL-33转基因小鼠伤后24小时相比,烧冲复合伤野生型C57BL/6小鼠趋化因子(CXCR2)明显减少；与各实验组相比,烧冲复合伤组小鼠血浆IL-6与TNF-α浓度均明显升高。
6.在烧伤、冲击伤、烧冲复合伤小鼠肺组织中IL-33的阳性细胞数与GRK2阳性细胞数、MPO阳性细胞数均有显著的正相关(r=0.65,p=0.042；r=0.638, p=0.0047；r=0.764,p=0.001)(r=0.716,p=0.02；r=0.661,p=0.0037；r=0.755, p=0.012),与Mv呈负相关(r=-0.677,p=0.031;r=-0.68,p=0.03;r=-0.816,p=0.004).
7.烧冲复合伤尸检见伤侧肺组织表面可见散在的斑片状出血,HE染色观察见大面积肺泡内出血。肺组织标本免疫组化染色见IL-33阳性细胞数高表达区域MPO阳性细胞数也高表达。
8.烧冲复合伤患者伤侧肺组织呈中度毛玻璃样变。
结论：
1.成功的建立了一种烧冲复合伤小鼠动物模型,具体参数为：野生型C57BL/6小鼠距离爆炸源53cm,压力峰值94Kpa致中度冲击伤,即刻将中度冲击伤小鼠背部脱毛区置入90℃沸水中持续9s,造成小鼠背部25%TBSAⅢ度烫伤。
2. IL-33通过激活GRK2通路阻断趋化因子CXCR2下调促进中性粒细胞迁移参与烧冲复合伤小鼠肺损伤。
3.高表达的IL-33参与烧冲复合伤患者肺损伤。
Objective:Burn-blast combined injury is one of the most common injuries in military conflict, terrorist attacks, traffic accidents, and other emergencies. Lung injury after burn-blast combined injury results in immediate death in up to47%of cases. Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are the main reasons for abrupt death in such injuries. Hypovolemic shock develops immediately after such injuries, initiating the generalized inflammatory cascade. Prior research in ALI and ARDS has demonstrated the importance of cytokines and neutrophils. Therefore, we focused on investigating cytokine-mediated neutrophils in the lungs after burn-blast combined injury. IL-33is a recently described member of the IL-1family, which also includes IL-1α/β, IL-1Ra, and IL-18. IL-33mRNA is expressed by multiple organs and cell types in humans and mice. IL-33protein is mainly expressed by epithelial cells, endothelial cells, and fibroblasts. IL-33attenuates sepsis by enhancing neutrophil influx to the site of infection. However, the function of IL-33-enhanced neutrophil influx in lung injury is unclear, specifically after burn-blast combined injury. Therefore, we established a burn-blast combined injury mice model. We investigated that IL-33would promote the participation of neutrophil migration in lung injury.
Methods:Burn-blast combined injury was induced in wild-type (WT) mice and IL-33transgenic mice. Mice were randomly divided into control group, burn group, blast group and burn-blast combined group. Immunohistochemistry assay was used to detect myeloperoxidase (MPO), IL-33, GRK2and CXCR2in lung after burn-blast combined group. Transmission electron microscopy (TEM) was used for observation of changes in lung. Plasma IL-6and TNF-a levels were measured by ELISA kits. Micro-CT was used for observation of changes in lung. In addition, Immunohistochemistry assay was used to detect myeloperoxidase (MPO) and IL-33in humans with burn-blast combined (BBLP). Chest radiograph scans was used to detect lung in humans with burn-blast combined.
Results:
1.We found that the mice at a distance of53cm, which exposed to94Ka peak overpressure, was the moderate blast injury distance when compared to mice at a distance of43cm and63cm, in these distances they were exposed200Ka and88.3Ka peak-overpressure, respectively.
2. The lungs of mice in burn-blast combined group (BBL) were severely congestive and most mice had more than5hemorrhage spots. However, the lungs of mice in burn (BU) or blast group (BL) showed less degree of congestion. In addition, the lungs of mice in control group (CO) were normal. The burn-blast combined injury group showed a significantly greater wet-to-dry weight ratio than the blast group and burn groups. The lung hemorrhage area in the burn-blast combined injury group was significantly higher than that for the blast injury and burn groups.
3. Burn-blast combined injury mice showed concomitantly reduced respiratory rate (Rr), tidal volume (Tv), minute ventilation volume (Mv), peak expiratory flow (PEF) as compared to burn injured mice, blast injured mice, and control mice at24hours. However, after burn-blast combined injury, WT mice exhibited significant lengthening of expiratory time (Te) and inspiratory time (Ti) as compared to each experimental group of WT mice at24hours.
4. We found moderate ground-glass shadows were seen in the left lung tissue in the burn-blast combined injury group on performing micro-CT. However, ground glass slightly appeared in various regions of left lung in the blast group and no lesions in the lung tissue of the control group and burn group.
5. MPO-, IL-33-and GRK2-positive cells significantly increased in the lung after burn-blast combined injury. However, the number of CXCR2-positive cells in WT mice was lower than those in the lungs of IL-33transgenic mice after burn-blast combined injury; Burn-blast combined injury mice had elevated plasma concentrations of IL-6and TNF-α.
6. In burn-blast combined injured IL-33transgenic mice, blast-injured IL-33transgenic mice, and burn-injured IL-33transgenic mice., some significant positive correlations were observed between IL-33-positive cells and both GRK2-positive cells (r=0.65, p=0.042; r=0.638, p=0.0047; r=0.764, p=0.001, respectively) and MPO-positive cells (r=0.716, p=0.02; r=0.661, p=0.0037; r=0.755, p= 0.012, respectively). The correlation coefficients suggested a strong association between IL-33-positive and Mv in burn-injured mice (r=-0.677, p=0.031), blast-injured mice (r=-0.68, p=0.03), and burn-blast combined injury mice(r=-0.816, p=0.004).
7. A large area of alveolar hemorrhage was seen in the patient with burn-blast combined injury. Interestingly, an increased number of MPO cells accumulated in the same area that IL-33is typically expressed.
8. Lung chest radiograph scans of the patient with burn-blast combined injury showed moderate ground-glass shadows in the left lung, while other areas appeared normal or nearly normal.
Conclusions:
1. We successfully established a stable mice model with burn-blast combined injury, which is inflicted with moderate blast injury by placing C57BL/6mice53cm away from explosive source, generating pressure peak of94Kpa, followed by induction of25%TBSA full-thickness burns on the back with90℃water for9s.
2. Our results suggest IL-33increases neutrophil influx to the site of infection and inflammation through GRK2pathway to block the downregulation of CXCR2with burn-blast combined injury.
3. Our results suggest that increased IL-33is involved in lung injury in humans with burn-blast combined injury.
引文
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