皮质醇对整合素家族细胞粘附分子CD11a/CD18、CD11b/CD18在大鼠急性坏死性胰腺炎合并多器官损伤白细胞表面表达的影响

我们应用流式细胞术检测了整合素家族细胞粘附分子CD11a/CD18和CD11b/CD18在大鼠急性坏死性胰腺炎(ANP)合并多器官损伤的模型血中白细胞表面的表达,探讨皮质醇在ANP合并多器官损伤中的作用及其机制。 一、材料与方法 1.动物模型制作方法:SD大鼠雌雄不拘,体重300～350g。随机分成ANP     

急性下肢深静脉血栓形成患者中性粒细胞CD11b/CD18及CD62L表达的研究

本实验旨在于研究外周血中性粒细胞CD11b／CD18及CD62L在急性下肢深静脉血栓形成（deep venous thrombosis，DVT）中的表达。     

严重烧伤大鼠早期外周血中性粒细胞CD11b/CD18分子的动态变化

为探讨烧伤后早期外周血中性粒细胞(PMN)膜上 CD11b/CD18分子的动态变化,采用大鼠30%TBSAⅢ度烧伤模型,伤后随机分为立即复苏组和延迟复苏组,于伤前及伤后12小时内的不同时间取血作流式细胞仪分析。结果表明:两组大鼠于伤后30分钟起 PMN CD11b/CD18表达就明显增加;立即复苏组于伤后4小时达到峰值;延迟复苏组在伤后1小时和8小时各有一个峰值,并比立即复苏组增高。认为烧伤后粘附分子 CD11b/CD18的变化可能与炎性介质、细胞因子、血流动力学改变引起的PMN 切应力的变化及缺血再灌注等密切相关。     

内毒素性肺损伤外周血中性粒细胞CD11b表达的意义

目的：探讨内毒素血症大鼠外周血中性粒细胞（PMN）表面CD11b表达与内毒素性肺损伤的关系。方法：大肠杆菌E-Coli O111B4 4mg／kg尾静脉注射制备大鼠内毒素血症动物模型。112只大鼠随机分为对照组（静脉注射等量生理盐水）及内毒素注射后1h组、2h组、4h组、8h组、12h组、24h组,每组16只动物。在相应时间点放血处死动物,分别取股静脉血、肺组织及进行支气管肺泡灌洗,测定肺组织湿／干重（W／D）比值、肺组织髓过氧化物酶（MPO）活性和支气管肺泡灌洗液（BALF）总蛋白定量等肺损伤指标。流式细胞仪测定外周血PMN表面CD11b表达。另取16只大鼠,内毒素注射后2h时测定外周血PMN表面CD11b表达,24h时放血处死,测定上述指标。结果：①大鼠内毒素血症可以造成明显的急性肺损伤,表现为肺组织W／D比值、MPO活性和BALF总蛋白明显增高,分别在2h、8h和2h显著高于对照组（P〈0．05或P〈0．01）,峰值分别出现在内毒素注射后12h、24h和12h;②大鼠内毒素性肺损伤时,外周血PMN表面CD11b表达水平在早期（1h）明显升高（与对照组比较,P〈O．05）,在2h达到峰值,之后逐渐降低;③外周血CD11b表达峰值明显早于肺组织W／D比、MPO和BALF总蛋白等肺损伤指标的峰值出现时间;④同一动物2h时外周血PMN表面CD11b的表达水平与其24h时肺组织W／D比、MPO和BALF总蛋白含量呈显著正相关（r分别为0．78、0．77和0．73,P〈0．05）。结论：内毒素性肺损伤中,外周血CD11b表达升高可能有助于内毒素性肺损伤的早期诊断,并可能预示以后的肺损伤程度。     

乌司他丁对原位肝移植术患者中性粒细胞CD11b/CD18表达的影响

目的探讨原位肝移植术中乌司他丁对中性粒细胞表面粘附分子CD11b／CD18表达的影响。方法择期行原位肝移植术患者4J0例，随机分为2组。乌司他丁组（U组，n=20）：切皮后开始持续静脉输注乌司他丁30万单位（加入100ml生理盐水中），每4小时重复一次；对照组（C组，n=20）：以等容量生理盐水代替。分别于切皮前即刻、切皮后120min、无肝期30min、新肝期60min和术毕采集外周静脉血1ml，采用流式细胞仪测定中性粒细胞表面粘附分子CD11b和CD18的表达。结果与切皮前比较，u组各时间点CD11b和CD18表达的差异无统计学意义，而C组新肝期60min和术毕时其表达明显上调（P＜0．01）。与C组比较，新肝期60minU组CD11b和CD18表达明显降低（P＜0．01）。结论乌司他丁可抑制原位肝移植术中患者CD11b／CD18表达的上调，有助于减轻炎性反应。     

CD11/CD18在烧伤早期中性粒细胞对内皮细胞粘附中的作用及变化

为了解烧伤早期病人中性粒细胞(PMN)膜表面 CD11a/CD18和 CD11b/CD18变化规律及其在烧伤早期 PMN 对内皮细胞(EC)粘附及损伤中的作用,为临床抗白细胞粘附治疗提供依据。将烧伤早期 PMN 与体外培养的人脐静脉内皮细胞(HUVEC)孵育24小时后,观察烧伤早期 PMN 与 EC 粘附百分率和烧伤早期 PMN 引起内皮细胞单层流出液生成速度(Jv)和滤过系数(kf)变化,CD11/CD18单抗(mAb)对烧伤早期 PMN-EC 粘附和内皮单层 kf、Jv 值影响。并应用流式细胞术检测烧伤病人伤后1周内 PMN 膜表面 CD11a/CD18和 CD11b/CD18的数量变化。结果显示严重烧伤病人伤后第1天 PMN细胞膜表面 CD11a/CD18和 CD11b/CD18明显升高达峰值,并在1周内仍维持于高水平。烧伤早期PMN 与 EC 粘附增加并可致内皮单层 kf、Jv 值明显升高,CD11a/CD18mAb 和 CD11b/CD18mAb 可降低粘附百分率70%～80%,并降低烧伤早期 PMN 诱导增高的内皮单层 kf、Jv 值(P<0.01)。提示烧伤后 PMN 迅速表达 CD11a/CD18和 CD11b/CD18,加强与 EC 间粘附,并可使内皮单层通透性增高,CD11a/CD18mAb 和 CD11b/CD18mAb 降低烧伤早期 PMN 与 EC 粘附,减轻烧伤早期 PMN 所导致的内皮单层通透性增高,从而保护内皮细胞。     

瑞芬太尼和异丙酚对健康成人静脉血中性粒细胞CD11b表达的影响

目的探讨瑞芬太尼和异丙酚对健康成人静脉血中性粒细胞（PMNs）CD11b表达的影响。方法取成人静脉血，采用正交实验设计确立实验因素为瑞芬太尼和异丙酚；实验水平数为5水平，即瑞芬太尼空白对照、溶媒（甘氨酸）对照、5ng／ml、50ng／ml、500ng／ml和异丙酚空白对照、溶媒（脂肪乳）对照、5μg／ml、50μg／ml、500／μg／ml，用正交表L25（5^6），观察药物对静息状态和脂多糖（LPS）激活状态PMNs下CD11b表达的影响，对激活状态的PMNs根据用药时机的不同又分为预防性用药和治疗性用药。预防性用药加入药物后1h用终浓度为1μg／ml的LPS进行刺激；治疗性用药在LPS刺激后1h加药。各标本均放入37℃、95％的空气-5％的CO2培养箱中孵育3h，其间每隔1h混匀1次。用流式细胞仪测定PMNs CD11b表达。结果瑞芬太尼和异丙酚对静息状态PMNs CD11b的表达无影响。预防性用药对PMNs CD11b表达的比较：与空白对照比较，5、50、500ng／ml瑞芬太尼可上调激活状态PMNs CD11b表达（P〈0．05或0．01）；与甘氨酸对照比较，50、500ng／ml瑞芬太尼可上调激活状态PMNs CD11b表达（P〈0．05和0．01）；异丙酚对激活状态PMNs CD11b表达无影响。治疗性用药对PMNs CD11b表达的比较：与空白对照和甘氨酸对照比较，500ng／ml瑞芬太尼可上调激活状态PMNs CD11b表达（P〈0．01）；与空白对照比较，50ng／ml异丙酚可上调激活状态PMNs CD11b表达（P〈0．05）。结论瑞芬太尼和异丙酚对PMNs的CD11b表达的影响可能与PMNs所处的状态、用药剂量以及用药时机有关。     

大承气汤对急性重型胰腺炎大鼠血中可溶性粘附分子CD11a/CD1 8表达的影响

目的：进一步认识大承气汤对急性胰腺炎的治疗机理。方法：采用胰管内逆行注入牛磺胆酸钠方法造成大鼠急性重型胰腺炎模型,造模后用大承气汤、生理盐水进行治疗,观察造模治疗后12h、14h动物血清中CD11a/CD18、淀粉酶及胰腺组织中TNF含量的变化和胰腺组织病理学的改变。结果：应用大承气汤治疗组的大鼠血中的可溶性CD11a/CD18表达胰腺组织中的TNF含量、胰腺组织病理损害程度、胰酶血症的水平均较生理盐水治疗组明显下降或减轻。结论：认为大承气汤治疗急性重型胰腺炎的机理可能不仅在于其能促进胰酶的排出,还与其减少粘附分子CD11a/CD18的表达,减少胰腺组织中PMNs的浸润程度,进而减轻了胰腺组织损伤有关。     

卡巴胆碱对肠缺血/再灌注大鼠中性粒细胞CD11b/CD18表达和血清可溶性细胞间黏附分子-1浓度的影响

目的:观察胆碱能激动剂卡巴胆碱对肠缺血/再灌注大鼠中性粒细胞(PMN)上CD11b/CD18表达和血清可溶性细胞间黏附分子-1(sICAM-1)浓度的调节作用。方法:54只雄性Wistar大鼠随机分为假手术组(N组)、肠缺血/再灌注组(GI/R组)及卡巴胆碱干预组(Car组)。采用夹闭肠系膜上动脉45min后恢复灌流的方法制成GI/R模型;卡巴胆碱组在肠缺血15min后经幽门注入卡巴胆碱(100μg/kg)。于肠缺血45min(I45)及再灌注1h(R1)、2h(R2)、6h(R6)取肠系膜上静脉血,双抗体夹心酶联免疫吸附(ELISA)法测定血清sICAM-1浓度,流式细胞仪检测PMN上CD11b/CD18表达率。结果:肠系膜上静脉血中PMN表面黏附分子CD11b/CD18的表达在肠缺血和再灌注后各时相点均增加(P<0.01),R2和R6时增加幅度较大;卡巴胆碱干预组R6时CD11b/CD18阳性PMN比例减少(P<0.05)。血清sICAM-1浓度在R1～R6时均升高(P<0.05),而给予卡巴胆碱的动物R6时降低(P<0.05),其值接近N组。结论:卡巴胆碱能降低肠缺血/再灌注大鼠PMN上CD11b/ C...     

异氟醚对大鼠全脑缺血再灌注时海马ICAM-1 mRNA和外周血中性粒细胞表面CD11b/CD18表达的影响

目的 探讨异氟醚对大鼠全脑缺血再灌注时海马组织ICAM-1 mRNA和外周血中性粒细胞表面CD11b/CD18表达的影响.方法 Wistar大鼠63只,随机分为3组(n=21):假手术组(S组)、缺血再灌注组(I/R组)和异氟醚组(Iso组).采用四血管阻断法制备全脑缺血再灌注模型.Iso组在四血管阻断过程中及再灌注早期吸入1.4%异氟醚.于再灌注6、24、72 h时,采集外周静脉血,采用流式细胞仪测定中性粒细胞表面CD11b/CD18和CD18的表达;RT-PCR法测定海马组织细胞间粘附分子-1(ICAM-1)mRNA和核因子κB(NF-κB)mRNA的表达.结果 与S组比较,I/R组再灌注6 h时CD11b/CD18和CD11b表达上调,再灌注24、72 h时ICAM-1 mRNA表达上调,I/R组和Iso组再灌注24 h时NF-κB mRNA表达上调(P＜0.05或0.01);与I/R组比较,Iso组再灌注6 h时CD11b表达下调,再灌注24 h时ICAM-1 mRNA表达下调(P＜0.05).结论 异氟醚可减轻大鼠全脑缺血再灌注损伤,可能与其抑制海马ICAM-1 mRNA及外周血中性粒细胞表面CD11b/CD18的表达有关.     

Hypertonic resuscitation modulates the inflammatory response in patients with traumatic hemorrhagic shock

OBJECTIVE: To determine the effect of resuscitation with hypertonic saline/dextran (HSD) on the innate immune response after injury. SUMMARY OF BACKGROUND DATA: Hypovolemic shock causes a whole body ischemia/reperfusion injury, leading to dysregulation of the inflammatory response and multiple organ dysfunction syndrome. Hypertonicity has been shown to modulate the innate immune response in vitro and in animal models of hemorrhagic shock, but the effect on the inflammatory response in humans is largely unknown. METHODS: Serial blood samples were drawn (12, 24, 72 hours and 7 days after injury) from patients enrolled in a prospective, randomized, double-blind trial of traumatic hypovolemic shock, HSD (250 mL) versus lactated Ringer's solution (LR) as the initial resuscitation fluid. Neutrophil (PMN) CD11b/CD18 expression was assessed via whole blood FACS analysis with and without stimulation (fMLP 5 micromol/L or PMA 5 micromol/L). PMN respiratory burst was assessed using the nitro-blue tetrazolium assay. Monocytes stimulated with 100 ng LPS for 18 hours were assessed for cytokine production (TNF-alpha, IL-1Beta, IL-6, IL-10, IL-12). RESULTS: Sixty-two patients (36 HSD, 26 LR) and 20 healthy volunteers were enrolled. CD11b expression, 12 hours after injury, was increased 1.5-fold in patients resuscitated with LR compared with controls. Those resuscitated with HSD had a significant reduction in CD11b expression 12 hours after injury, compared with LR. There was no difference in respiratory burst early after injury. Monocytes from injured patients expressed lower levels of all cytokines in comparison to normal controls. Patients give HSD showed a trend toward higher levels of IL-1beta and IL10 production in response to LPS, 12 hours after injury. CONCLUSION: HSD resuscitation results in transient inhibition of PMN CD11b expression and partial restoration of the normal monocyte phenotype early after injury.     

急性坏死型胰腺炎大鼠肠粘膜CD44 mRNA的表达及生长激素的作用

目的 观察急性坏死型胰腺炎（ANP）大鼠肠粘膜CD44 mRNA表达、并探讨其与肠粘膜T淋巴细胞亚群和病理形态学变化的关系及生长激素（GH）的作用。方法 SD大鼠54只，随机分为3组：假手术组（SO）；ANP组；ANP＋GH组（0．75U／kg体重）。大鼠胰胆管内逆行推注5％牛磺胆酸钠溶液（1ml/kg体重）制备ANP模型。术后6、12、24h分批处死。逆转录聚合酶链反应研究CD44 mRNA的表达。免疫组织化学观察肠粘膜T淋巴细胞亚群。结果 ANP组各时点CD44 mRNA表达较SO组显著降低（P＜0．05）。GH上调CD44 mRNA的表达。ANP组术后6、12、24h肠粘膜CD3、CD4、CD8细胞数较SO组显著减少（P＜0．05），而GH治疗组肠粘膜CD3、CD4、CD8细胞数与SO组差异无差异性（P＞0．05）。ANP组肠上皮破损明显，GH治疗组肠粘膜结构基本完整。结论 ANP大鼠肠粘膜CD44 mRNA表达降低，而GH维持肠粘膜上皮结构完整及粘膜免疫功能的作用可能与上调CD44 mRNA表达有关。     

Factors in intestinal lymph after shock increase neutrophil adhesion molecule expression and pulmonary leukosequestration

BACKGROUND: Because the ischemic gut may produce factors that initiate systemic inflammation, we tested the hypothesis that factors released from the gut into the mesenteric lymphatics increase neutrophil (PMN) adhesion molecule expression after trauma and shock. METHODS: At 1 and 4 hours after hemorrhagic shock (30 mm Hg x 90 minutes) plus trauma (laparotomy) (T/HS) or sham-shock (T/SS), with or without mesenteric lymph duct ligation, PMN CD11b and CD18 expression was assessed in male rats. In additional rats, mesenteric lymph samples were tested for their ability to increase PMN CD11b expression in vitro. Lastly, at 4 hours after T/SS or T/HS with or without lymph duct ligation, pulmonary PMN sequestration was measured. RESULTS: Compared with T/SS rats, T/HS was associated with up-regulation of PMN CD11b and CD18 expression, which was largely prevented by ligation of the mesenteric lymph duct (p < 0.01). Lymph duct ligation also prevented T/HS-induced pulmonary leukocyte sequestration (p < 0.01). In addition, mesenteric lymph from rats subjected to T/HS but not T/SS increased CD11b expression (p < 0.01). CONCLUSION: Factors produced or released by the postischemic intestine and carried in the mesenteric lymph appear responsible for PMN activation and pulmonary PMN sequestration after an episode of T/HS.     

CO_2气腹对大鼠重症急性胰腺炎胰腺病理及IL-1、IL-6、CD11a/CD18和CD11b/CD18的影响

目的研究腹腔镜手术时CO2气腹对Sprague-Dawley(SD)大鼠重症急性胰腺炎(SAP)胰腺组织病理学改变、血淀粉酶、炎症细胞因子(IL-1和IL-6)和可溶性黏附分子(CD11a/CD18和CD11b/CD18)的影响。方法雄性SD大鼠50只,随机分为3组:CO2气腹组(n=20),5%牛磺胆酸钠胆胰管逆行注射方法制备SAP动物模型后,以气腹机向大鼠腹腔内注入CO2〔压力12mmHg(1mmHg=0.133kPa),维持30min〕;SAP组(n=20):建立SAP模型后关腹,不充入CO2;单纯手术组(n=10):仅开腹翻动胰腺后关腹。各组均于术后2.5h处死动物,取静脉血测定血淀粉酶、IL-1和IL-6水平及CD11a/CD18和CD11b/CD18的表达阳性率,并进行胰腺组织病理学检查。结果与单纯手术组相比,CO2气腹组和SAP组胰腺组织病理学评分、血清淀粉酶、IL-1和IL-6水平及CD11a/CD18和CD11b/CD18表达阳性率均明显升高,差异有统计学意义(P=0.000)。与SAP组相比,CO2气腹组血IL-1和IL-6水平明显降低,差异有统计学意义(P=0.000);而胰腺组织病理学评分(P=0.294)、血清淀粉酶水平(P=0.073)、CD11a/CD18(P=0.155)和CD11b/CD18(P=0.201)表达阳性率的差异无统计学意义。结论对于SAP大鼠,CO2气腹对IL-1和IL-6水平有一定的抑制作用;而对胰腺病理变化及CD11a/CD18和CD11b/CD18表达阳性率无明显影响。     

羟乙基淀粉对内毒素血症大鼠肠系膜细静脉白细胞活化和血管通透性的影响

目的 探讨羟乙基淀粉(HES 130/0.4)对内毒素血症早期大鼠肠系膜细静脉白细胞活化及血管通透性的影响.方法 雄性Wistar大鼠36只,体重200～250 g,随机分为3组(n=12):对照组(C组)静脉注射生理盐水0.5 ml后,静脉输注生理盐水16 ml·kg-1·h-1;内毒素组(LPS组)静脉注射LPS 2 mg/ks(溶于生理盐水0.5 ml)后,静脉输注生理盐水16 ml·kg-1·h-1;HES组静脉注射LPS 2ms/kg(溶于生理盐水0.5 ml)后,静脉输注HES 16 ml·kg-1·h-1.各组补液时间60 min.观察给药前及补液期间和补液后30 min内肠系膜细静脉白细胞滚动数、粘附数、游出数、肥大细胞脱颗粒情况及细静脉血管通透性情况,检测外周血白细胞粘附分子CD11b和CD18的表达.结果 与C组比较,LPS组沿肠系膜细静脉内滚动、粘附和游出的白细胞增加,肥大细胞脱颗粒率增加,LPS组和HES组CD11b、CD18表达上调,细静脉血管通透性增加(P＜0.05).与LPS组比较,HES组上述指标均降低(P＜0.05).结论 HES 130/0.4可抑制内毒素血症早期大鼠肠系膜细静脉白细胞沿血管壁滚动、粘附和游出,抑制肥大细胞脱颗粒及血管通透性的增加,从而改善微循环障碍.     

Endotoxin suppresses matrix protein-induced upregulation of PMN candicidal activity: an effect reversed by low-dose TNF-alpha.

We investigated the relationship of polymorphonuclear leukocyte (PMN) candicidal activity, matrix proteins, and lipopolysaccharide (LPS) to determine how LPS modulates the normal enhancing effect of matrix proteins on PMN candicidal activity. LPS reduced PMN candicidal activity when PMN were adhered in the presence of either fibronectin or laminin. In the presence of fibronectin or laminin, LPS reduced CD11b/CD18 expression (the fibronectin receptor) as assessed using sheep erythrocytes coated with C3bi. Experiments with 125I-fibronectin and 125I-RGDS (Arg-Gly-Asp-Ser) demonstrated that LPS reduced both the binding of fibronectin and the bioavailability of the binding epitope on the PMN surface. Stimulating the PMN oxidative burst with PMA but not FMLP also reduced fibronectin and RGDS binding. Incubation of LPS-treated PMN with staurosporine blocked the decrease in fibronectin and RGDS binding. Exposure of PMN to LPS plus low-dose TNF-alpha restored both fibronectin and RGDS binding with a concomitant increase in CD11b/CD18 surface expression. Low-dose TNF-alpha restored PMN candicidal activity in the presence of LPS and was most effective if PMN were preadhered to fibronectin. These results demonstrate that: (1) matrix proteins enhance normal PMN candicidal activity, (2) LPS reduces PMN candicidal activity in the presence of matrix proteins, (3) stimulation of the PMN oxidative burst in particular via protein kinase c activation reduces the bioavailability of the fibronectin receptor, and (4) low-dose TNF-alpha may restore PMN candicidal activity in part by upregulating the surface receptor for fibronectin binding.     

烧伤后白细胞与内皮细胞粘附分子介导作用的研究

为研究白细胞粘附依赖于细胞粘附分子的介导作用,作者通过离体实验观察分析了烧伤血清对外周血中性粒细胞（ＰＭＮ）ＣＤ１１ｂ／ＣＤ１８表达的影响及ＣＤ１１ｂ／ＣＤ１８在烧伤后ＰＭＮ粘附中的介导作用。结果表明：（１）烧伤血清使ＰＭＮＣＤ１１ｂ／ＣＤ１８分子表达和ＰＭＮ与肺微血管内皮细胞（ＰＭＥＣ）的粘附率增高。（２）ＣＤ１１ｂ／ＣＤ１８单抗不仅能使正常ＰＭＮ与ＰＭＥＣ的粘附率下降５０％,也使烧伤血清激活的ＰＭＮ与ＰＭＥＣ粘附率下降至烧伤血清激活前水平。我们认为,严重烧伤能使外周血ＰＭＮＣＤ１１ｂ／ＣＤ１８表达明显增高,ＣＤ１１ｂ／ＣＤ１８不但介导基础状态下的ＰＭＮ粘附,更是介导烧伤后引起的大量ＰＭＮ与ＰＭＥＣ粘附的主要分子。     

Modulation of human leukocyte antigen-DR on monocytes and CD16 on granulocytes in patients with septic shock using hemoperfusion with polymyxin B-immobilized fiber

BACKGROUND: Hemoperfusion with PMX-F (polymyxin B covalently immobilized on fibers) has been reported to be safe and effective for patients with septic shock. However, the molecular mechanism of this usefulness is not yet clear. The purpose of this study was to evaluate whether the expression of CD14, human leukocyte antigen (HLA)-DR on monocytes, and the expression of CD16, CD11b/CD18 on neutrophils, are altered in septic patients according to the severity, and whether PMX-F treatment affects the clinical parameters and the expression of leukocyte surface antigen expression. PATIENTS AND METHODS: Thirty-four patients who were taken to the National Defense Medical College hospital at emergency, and who had an identified focus of infections, were enrolled in this study. The patients were divided into three groups: non-systemic inflammatory response syndrome [SIRS]) group, sepsis group, and septic shock group. Peripheral blood samples were collected at the time of admission to our hospital. The CD14, HLA-DR expression on monocytes and the CD11b/CD18, CD16 expression on granulocytes were evaluated using flowcytometry, and the serum interleukin (IL)-6 and IL-10 levels were measured using enzyme-linked immunosorbent assay. Treatment with a PMX-F column was performed in 10 patients with septic shock. RESULTS: The HLA-DR expression on monocytes and the CD16 intensity on granulocytes in patients with septic shock were significantly lower than those in patients with sepsis. The serum IL-6 and 10 levels in patients with septic shock were significantly higher than those in patients with sepsis. The mean systolic blood pressure in patients with septic shock was significantly increased after the PMX-F treatment; furthermore, the HLA-DR expression on monocytes and the CD16 intensity on granulocytes were significantly increased after the PMX-F treatment. The serum IL-10 levels were significantly decreased after the PMX-F treatment. CONCLUSIONS: We showed that the surface antigens, HLA-DR on monocytes and CD16 on granulocytes, are extremely decreased in patients with septic shock, and that PMX-F treatment is effective for beneficially increasing the surface antigen expression on leukocytes. This therapy might be a new strategy for helping patients recover from immunoparalysis in septic conditions.