Expression of adhesion molecules in chronic serum sickness in rats

Peripheral blood leukocytes infiltrate the kidney in chronic serum sickness (CSS). We therefore studied the expression of CD54 and its ligands CD18 and CD11b/c in CSS in 10 rats with CSS, 6 rats immunized similarly who did not developed proteinuria (no-CSS group), and 10 normal rats (control group). Intense (6 to 35 times more than controls) leukocyte infiltration was observed in CSS. The CSS group over-expressed CD54 in glomeruli and interstitium in association with increments in CD18- and CD11b/c-positive cells ranging 2.5 to 7 times the number found in controls. 75% of infiltrating leukocytes expressed CD18 and 87% expressed CD11b/c. The non-CSS group had leukocyte infiltration and expression of adhesion molecules similar to control group. Adherence of CD43-positive cells to renal tissues was 4 times higher in renal tissue from CSS rats than to normal kidney. Pretreatment with corresponding Mabs reduced adherence by half. We concluded that over-expression of CD54 and its ligands CD18 and CD11b/c in infiltrating leukocytes occur in CSS. Binding experiments suggest the functional relevance of these molecules.     

同型半胱氨酸增强血白细胞粘附分子的表达

用免疫荧光流式细胞仪检测同型半胱氨酸是否改变体外健康人血单核细胞,中性粒细胞,及淋巴细胞表达粘附分子CD11b,CD18和L－选择素（L-selectin)的表达。结果显示,同型半胱氨酸在低浓度20μmol/L时明显增加CD11b和CD18在各种白细胞表面的表达,同时也增加了CD14在单核及中性粒细胞的表达。这种作用随同型半胱氨酸浓度升高而增强,但当浓度升至等于或大于1mmol/L时,各种粘附分子的表达反而降低。同型半胱氨酸使各种细胞类型表面L-selectin降低。此结果表明同型半胱氨酸可改变白细胞表面粘附分子的表达,可能在体内通过此途径导致白细胞粘附并游出血管内皮。     

Effect of blood temperature on the efficacy of systemic leucodepletion during cardiopulmonary bypass: a prospective randomized clinical study

The authors examined the effect of blood temperature within the cardiopulmonary bypass (CPB) circuit on the efficacy of an arterial line filter. Eighty patients undergoing elective, primary coronary artery bypass grafting under CPB were prospectively randomized in two equal groups. Blood temperature was kept at 35 degrees C in the first group and reduced to 28 degrees C in the second group. Twenty patients in each group had an arterial line LG6 filter attached onto CPB circuit. The other 20 patients in each group (controls) had a non-leukocyte-depleting filter. Blood samples (10 ml) were taken before CPB, at 5 minutes on CPB, at 30 minutes on CPB, 5 minutes after aortic clamp removal, and 6 hours postoperatively. Leucocytes were counted under light microscopy. Activated leucocytes were identified using nitroblue tetrazolium staining. Patients undergoing leucodepletion had significantly lower total and activated leukocyte counts than control patients in both groups (p < 0.05). Patients having a leukocyte-depleting filter at a CPB temperature of 35 degrees C had significantly lower total leukocyte counts (p < 0.05) than those having a leukocyte-depleting filter at a CPB temperature of 28 degrees C (p < 0.05). However, there were not statistically significant differences in the activated leukocyte counts between the two leucodepleted groups (p > 0.05). This study shows that warm blood temperature within the CPB circuit has a positive effect on the overall leucodepleting efficacy of the LG6 filter. Activated leucocytes, however, seem to be depleted at similar rates irrespective of the blood temperature in the CPB circuit.     

地奥司明对肾缺血再灌注大鼠肾组织MPO和中性粒细胞CD11b、CD54及CD62L水平的影响

 目的：观察地奥司明（DOSM）对肾缺血/再灌注（I/R）大鼠肾组织髓过氧化物酶（MPO）和中性粒细胞CD11b、CD54及CD62L表达水平的影响。方法: 180只SD大鼠随机分成3组:假手术组(SO)、肾缺血/再灌注模型组(I/R)和地奥司明+肾缺血/再灌注模型组(DOSM+I/R)。采用ELISA方法测定肾脏组织中MPO的水平,流式细胞分析法检测中性粒细胞表面CD11b、CD54和CD62L的表达水平。结果: 在1h、3h、6h、12h、24h和48h不同时间点的肾组织中,I/R和DOSM＋I/R两组MPO活性均随时间逐渐升高,于6h达最高,后逐渐下降,两组相比有显著性差异（P＜0.05或P＜0.01）。中性粒细胞CD11b、CD54及CD62L的表达在相同时段I/R组显著高于SO组（P＜0.05或P＜0.01);而在DOSM+I/R组显著低于I/R组（P＜0.05或P＜0.01)。结论：DOSM可显著降低肾I/R病理过程中MPO活性,显著降低中性粒细胞CD11b、CD54及CD62L的表达,有助于减轻I/R时炎性细胞的浸润。     

Expressions of selected adhesion molecules on peripheral blood leukocytes in patients with aggressive periodontitis

INTRODUCTION: Aggressive forms of periodontitis lead to rapid bone destruction resulting in extensive losses in children's and young adults' dentition. Adhesion molecule deficiency syndrome and abnormalities in the expression of various adhesion molecules on peripheral blood leukocytes can be observed in prepubertal and aggressive periodontitis (AP) patients. The aim of the study was thus to assess the expression of selected cell adhesion molecules (CAMs; CD11a, CD11b, CD11c, CD54, and CD62L) on monocytes, neutrophils, and lymphocytes of the peripheral blood in patients with AP. MATERIAL/METHODS: The study involved 16 patients with AP and a control group of 13 generally healthy subjects with healthy periodontium. CAM expressions were determined by flow cytometry and presented as mean fluorescence intensity (MFI) and percentage of cells showing expression of the assessed adhesion molecules. RESULTS: Neutrophil CAM expressions in AP patients were comparable with those of the control group. MFI of CD62L on monocytes in AP patients was significantly lower than that of the controls. Lymphocytes showed increased CD11b expression compared with the control group. The percentage of leukocytes showing CAM expression in both groups was similar. Only the percentage of lymphocytes with CD11b in AP patients was significantly higher than in healthy controls. CONCLUSIONS: Because of the evident lack of differences between patients and controls and the great amount of individual dispersion of the results, the above CAMs on peripheral blood leukocytes in generally healthy patients with AP do not seem to be characteristic markers of this disease.     

Outer membrane vesicles from Neisseria meningitidis

Flow cytometry was used to study the expression of leukocyte adhesion molecules CD11a, CD11b, CD11c, CD14, and CD62L (L-selectin) and production of reactive oxygen species (ROS) in an ex vivo human whole-blood system stimulated with lipopolysaccharide-containing outer membrane vesicles (LPS-OMV) from N. meningitidis. Results demonstrated a dose-dependent increase in surface expression of CD11a, CD11b, CD11c and CD14 in granulocytes and monocytes (maximal at 30-120 min) upon OMV-LPS challenge, whereas CD62L expression was heavily downregulated (maximal at 30-120 min). The OMV-associated LPS was almost as potent (on a weight basis) as purified LPS from E. coli in inducing adhesion molecule modulation but the response was delayed. Upon stimulation with OMV-LPS or E. coli-LPS, the production of intracellular ROS increased in both granulocytes and monocytes when dihydroethidium (DHE, mainly reflecting superoxide anion) was used as a probe, whereas peroxynitrite production monitored with dihydrorhodamine 123 (DHR) was not significantly changed. The OMV-mediated modulation of leukocyte adhesion molecule expression and increased ROS production may certainly lead to increased entrapment of leukocytes in the microcirculation and contribute to untoward inflammatory reactions as seen in systemic meningococcal disease.     

Influence of graded magnesium deficiencies on white blood cell counts and lymphocyte subpopulations in rats.

Increased white blood cell counts or leukocytosis have been observed primarily in young rats fed diets extremely low in Mg (< 60 ppm) and high in phosphorus (0.5 % P). We investigated the influence that acute and moderate Mg deficiencies have on blood leukocytes at high and low dietary phosphorus levels. For four weeks, male Sprague-Dawley rats (initially 7 weeks old) were fed diets containing 30, 60, 120, 208, or 850 ppm Mg and either 0.3 % or 0.5 % dietary phosphorus. Total leukocytes were increased in rats fed 30 ppm Mg (p < 0.0001), and the leukocyte subpopulation counts of lymphocytes, neutrophils, monocytes and eosinophils increased significantly only in the rats fed 30 ppm Mg (p < 0.0001). B-cells decreased significantly as a percentage of lymphocytes (p < 0.0093) as dietary Mg decreased. As total counts in blood, B-cells, CD4 and CD8 cells were significantly increased in the rats consuming the 30 ppm Mg diet. Dietary phosphorus only had an effect in combination with the lowest dietary Mg. These results demonstrate a threshold effect for increased leukocytes during a Mg deficiency of four weeks. A Mg deficiency of a longer duration may show different results.     

A rare association between leukocyte adhesion deficiency type I and psoriasis in humans

The β2 integrins are expressed exclusively on leukocytes and participate in many immune and inflammatory processes. This subfamily comprises four heterodimeric glycoproteins with a common β-subunit, designated β2 (CD18). Spontaneous mutations of the CD18 gene result in leukocyte adhesion deficiency type I (LAD-I). Low level of CD18 expression has also been implicated in the pathogenesis of psoriasis. We here describe a child with recurrent skin infections without pus formation, persistent gingivitis and periodontitis. His blood counts showed persistent leukocytosis (neutrophilia). CD11b expression was defective on neutrophils, while that of CD18 was normal. So, our patient represents a mild variant of LAD-I with possible dysfunctional CD18. Moreover, he developed psoriasis with reduced CD18 expression on CD4(+) T-cells. Psoriasiform dermatitis has been described before in association with LAD-I, however, clinically and histologically confirmed psoriasis in association with LAD-I has been described only in CD18 hypomorphic mice. Therefore, our patient represents the first clinically and histopathologically documented association between LAD-I and psoriasis in humans. It lends support to the role of β2 integrins in the etiopathogenesis of psoriasis.     

Changed expression of leukocyte adhesion molecules and increased production of reactive oxygen species caused by Streptococcus pyogenes in human whole blood

To elucidate the innate immune responses to group A streptococci (GAS) important in the pathophysiology of sepsis, flow cytometric techniques were applied to study the effects of live and heat-inactivated GAS, including their particulate and soluble components, on the expression of leukocyte adhesion molecules CD11b (Mac-1) and CD62L (L-selectin), and leukocyte production of reactive oxygen species (ROS) in human whole blood. GAS caused marked time- and concentration-dependent increases in CD11b and ROS, while CD62L was downregulated. Live and heat-inactivated GAS induced similar changes in leukocyte adhesion molecules, whereas ROS production induced by heat-inactivated GAS (and its particulate fraction) was 4 (2.5)-fold higher than with live GAS. Leukocyte nitric oxide production (24 h) was not enhanced. Although GAS proved a more potent inducer of ROS production, leukocyte responses to GAS were similar to those reported for lipolysaccharides, indicating that Gram-positive and Gram-negative bacteria activate common pathways in the inflammatory response. High ROS production may contribute to tissue damage caused by GAS.     

In vitro hemocompatibility studies of drug-loaded poly-(L-lactic acid) fibers

Our objective was to evaluate the hemocompatibility of biodegradable stent fibers, employing a closed-loop circulation system filled with human blood. We also investigated the effects of the anti-inflammatory and anti-proliferative drugs curcumin and paclitaxel, incorporated into stent fibers. Fresh whole blood was circulated in four parallel closed-loop systems: the empty tube circuit (control) and tubes containing either a PLLA fiber coil (PLLA), a curcumin-loaded PLLA coil (C-PLLA) or a paclitaxel-loaded PLLA coil (P-PLLA). The influence of PLLA fiber, alone or loaded with drug incorporated during melt-extrusion, on leukocyte and platelet adhesion and activation was determined by flow cytometry. The effects of blood flow and fiber properties on cell deposition were assessed by scanning electron microscopy (SEM). The flow cytometry results clearly demonstrated that PLLA triggers blood cell activation at the site of deployment, as shown by increases in CD11b, CD62P and leukocyte-platelet aggregates, compared to controls. Curcumin and paclitaxel treatments both significantly reduced leukocyte and platelet activation and adhesion to PLLA fibers, as shown by flow cytometry and SEM. Activated leukocytes and platelets revealed significantly lower CD11b and CD62P receptor binding for C-PLLA compared with PLLA alone, and slightly lower for P-PLLA. Reductions in platelet-leukocyte aggregates were observed as well. In addition, there was less leukocyte and platelet adhesion to C-PLLA, compared with PLLA fiber controls, as shown by SEM. A continuous linear thrombus, composed of platelets, leukocytes, red blood cells and fibrin was occasionally detected along the line of tangency between the coil and the tube wall. Flow separation and eddying, proximal and distal to the line of tangency of coil and tube, is thought to contribute to this deposit. Curcumin was more effective than paclitaxel in reducing leukocyte and platelet activation and adhesion to PLLA stent fibers in this setting. However there was evidence of paclitaxel degeneration during melt extrusion that may have inhibited its effectiveness. Incorporation of the anti-inflammatory and anti-proliferative drug curcumin into bioresorbable stent fibers is proposed to prevent thrombosis and in-stent restenosis.     

急性淋巴细胞白血病细胞β2整合素及L-选择素的表达与意义

目的和方法:研究急性淋巴细胞白血病(ALL)细胞粘附分子β₂整合素(CD11a、CD11b)及L-选择素(CD62L)的表达及其临床意义。用流式细胞仪检测45例ALL及25例正常人骨髓单个核细胞的CD11a、CD11b、CD62L表达。结果:①CD11a、CD11b在ALL细胞上表达均明显低于正常人,CD11b低表达的阳性率为100%,50%患者有CD11a低表达。而60%患者CD62L在ALL细胞上表达升高。②CD11a在B-ALL表达明显低于T-ALL表达,CD62L在B-ALL表达高于T-ALL。③浸润组CD11a表达高于非浸润组(P＜0.05)。④ALL完全缓解组CD11a、CD11b的表达在正常范围。结论:急性淋巴白血病细胞上存在多个粘附分子的表达异常,检测粘附分子有助于判断白血病细胞类型及疗效。     

高脂血症循环白细胞自发活化作用的研究

高血脂是心脑血管病的重要危险因素。活化白细胞在缺血过程中微血管嵌塞和组织损伤中起重要作用。为了研究血清胆固醇对循环白细胞活化作用的影响，采用硝基蓝四唑试验测量了高脂血症家兔循环白细胞自发活化率（SAR）。结果指出，高脂血症动物循环白细胞SAR（％）显著高于对照组（P＜0.01）。SAR升高与血清胆固醇水平有关。循环白细胞SAR升高导致白细胞粘附分子CD11／CD18表达增加和微循环障碍。因此循环白细胞SAR升高是心脑血管病重要危险因素之一。     

Leukocyte activation and function-associated antigens in inflammatory disease

Expression of adhesion molecules, CD11a, CD11b and CD18, and of the function-associated molecules CD3, CD4, CD8, CD16, CD19, CD56 and CD57 was assayed on peripheral blood leukocytes from normal control subjects (n=10), and from patients with adult periodontitis PD (n=9), ankylosing spondylitis AS (n=11) and rheumatoid arthritis RA (n=14). A novel rapid fixation leukocyte preparation technique was used which prevents artefactural up-regulation of surface antigens.In RA patients, the percentage of CD18+ lymphocytes was decreased and that of CD11b+ neutrophils was increased. On lymphocytes the mean fluorescence intensity (MFI) of both CD11b and CD18 was decreased whereas that of CD57 was increased. In AS patients the percentages of CD11b+ lymphocytes and neutrophils were increased and CD18+ lymphocytes and neutrophils were decreased. On lymphocytes the MFIs of CD11b and CD18 were decreased, whilst that of CD16 was increased. On neutrophils the MFI for CD18 was increased. No significant differences (p<0.01) were seen for the periodontitis patients. It is suggested that the antigen expression on peripheral blood cells from RA and AS patients is consistent with leukocyte activation.     

急性坏死性胰腺炎大鼠白细胞L-选择素表达和肌动蛋白分布的变化及中药华西胰腺炎一号的影响

目的： 了解胰腺局部循环内白细胞在急性坏死性胰腺炎（ANP）疾病过程中L-选择素的表达及肌动蛋白纤维多聚体（F-actin）在细胞内的分布特点,并探讨中药华西胰腺炎一号（WPY）对它们的影响。方法：44只Wistar大鼠分为正常、ANP组及ANP WPY治疗组,脾静脉采血, 予CD62L单抗标记粒细胞L-选择素,TRTIC-Phalloidin标记白细胞F-actin,流式细胞仪检测粒细胞中的CD62L阳性细胞数,共聚焦激光扫描显微镜采集白细胞图像并对F-actin在白细胞内的分布进行分析。结果：ANP组脾静脉血中CD62L阳性细胞数明显高于正常对照组（11.96%±5.32%）, 6 h（31.78%±12.37%）、12 h(29.83%±13.73%)与对照组比较差异显著（P<0.05）,WPY治疗组6 h CD62L阳性细胞数低于ANP组。白细胞F-actin细胞边缘与中央灰度比在ANP各时段,除3 h外均增高,1 h(2.52±0.49)、12 h(2.72±0.48)与对照组比较有显著差异（P<0.05）, WPY治疗组6 h（1.54±0.24）明显低于ANP组（2.35±0.55）（P<0.05）。结论： ANP胰腺局部循环内白细胞L-选择素的表达及F-actin分布发生明显改变,提示白细胞黏附特性改变及变形能力下降是ANP病情进展的重要病理生理因素之一,中药华西胰腺炎一号对它们有一定的影响。     

重症烧伤休克大鼠白细胞表面beta-2整合素的表达

目的 :阐明烧伤休克时 beta-2整合素与白细胞 -内皮细胞粘附间的关系。方法 :将 16只 SD大鼠随机均分为对照组和烧伤休克组。应用流式细胞技术检测中性粒细胞及单细胞表面 beta-2整合素CD11a( LFA-1)和 CD11b( Mac-1)的表达量变化 ,同时比较观察二组动物肠系膜微循环中微静脉内白细胞与内皮细胞粘附数量变化。结果 :二组自身对照 (烫伤前与烫伤后 3 h或开腹前与开腹后 3 h)及相互对比结果显示 ,中性粒细胞及单核细胞表面 CD11a表达量均无显著差异 ( P>0 .0 5 ) ;在烧伤组 ,单核细胞 CD11b有显著降低( P<0 .0 5 ) ,而中性粒细胞 CD11b有显著升高 ( P<0 .0 5 )。微循环观察结果显示 ,休克组动物烫伤后随时程延长附壁滚动及紧密粘附的白细胞数量明显增多 ,而对照组则无明显变化。结论 :烧伤休克状态下 ,白细胞表面 CD11a数量无显著变化 ,而 CD11b数量则有所改变。白细胞 -内皮细胞粘附力的增强可能有 beta-2整合素功能活性上调参与。     

Leukocyte activation and function-associated antigens in inflammatory disease

Expression of adhesion molecules, CD11a, CD11b and CD18, and of the function-associated molecules CD3, CD4, CD8, CD16, CD19, CD56 and CD57 was assayed on peripheral blood leukocytes from normal control subjects (n=10), and from patients with adult periodontitis PD (n=9), ankylosing spondylitis AS (n=11) and rheumatoid arthritis RA (n=14). A novel rapid fixation leukocyte preparation technique was used which prevents artefactural up-regulation of surface antigens.In RA patients, the percentage of CD18+ lymphocytes was decreased and that of CD11b+ neutrophils was increased. On lymphocytes the mean fluorescence intensity (MFI) of both CD11b and CD18 was decreased whereas that of CD57 was increased. In AS patients the percentages of CD11b+ lymphocytes and neutrophils were increased and CD18+ lymphocytes and neutrophils were decreased. On lymphocytes the MFIs of CD11b and CD18 were decreased, whilst that of CD16 was increased. On neutrophils the MFI for CD18 was increased. No significant differences (p<0.01) were=" seen=" for=" the=" periodontitis=" patients.=" it=" is=" suggested=" that=" the=" antigen=" expression=" on=" peripheral=" blood=" cells=" from=" ra=" and=" as=" patients=" is=" consistent=" with=" leukocyte=">     

Biological performance of a novel synthetic furanone-based antimicrobial

Infection of medical devices causes significant morbidity and mortality and considerable research effort has been directed at solving this problem. The aim of this study was to assess the biological performance of a novel furanone compound that has potential as an anti-infective coating for medical devices. This study examined in vitro leukocyte response following exposure to the antibacterial 3-(1'-bromohexyl)-5-dibromomethylene-2(5H)-furanone and assessed the tissue response following subcutaneous implantation of the furanone compound covalently bound to polystyrene (PS). Peripheral human blood was exposed to furanones in solution for 1h and flow cytometry used to analyse viability and changes in expression of surface receptors CD11b/CD18 and CD44. Flow cytometry results from propidium iodide stained cell suspensions suggested that the leukocytes were viable after exposure to furanones in whole blood. No significant difference was found in the expression of CD11b/CD18 and CD44 between the furanone exposed samples and the negative control for neutrophils suggesting that the furanones themselves do not activate these leukocytes. The positive control lipopolysaccharide significantly up-regulated CD11b/CD18 and slightly down-regulated CD44 on both PMNs and monocytes. In vivo studies of the tissue response to furanone covalently bound to PS showed that there was no significant difference in cellularity of capsules surrounding the disk and no significant increase in myeloperoxidase expression. These results demonstrate negligible acute inflammatory response to synthetic brominated antibacterial furanones. Future studies will focus on chronic responses and examination of in vivo efficacy.     

Severe meningococcal disease is characterized by early neutrophil but not platelet activation and increased formation and consumption of platelet-neutrophil complexes

Approximately 25% of polymorphonuclear leukocytes (PMNL) circulate in heterotypic complexes with one or more activated platelets. These platelet-neutrophil complexes (PNC) require platelet CD62P expression for their formation and represent activated subpopulations of both cell types. In this study, we have investigated the presence, time course, and mechanisms of PNC formation in 32 cases of severe pediatric meningococcal disease (MD) requiring intensive care. There were marked early increases in PMNL CD11b/CD18 expression and activation, and reduced CD62L expression compared with intensive care unit control cases. Minimal platelet expression of the active form of alphaIIbbeta3 (GpIIb/IIIa) was seen. PNC were reduced on presentation and fell to very low levels after 24 h. Immunostaining of skin biopsies demonstrated that PNC appear outside the circulation in MD. In vitro studies of anticoagulated whole blood inoculated with Neisseria meningitidis supported these clinical findings with marked increases in PMNL CD11b/CD18 expression and activation but no detectable changes in platelet-activated alphaIIbbeta3 or CD62P expression. In vitro PMNL activation with N. meningitidis (or other agonists) potentiated the formation of PNC in response to platelet activation with adenine diphosphate. Therefore, in severe MD, PMNL activation is likely to promote PNC formation, and we suggest that the reduced levels of PNC seen in established MD reflect rapid loss of PNC from the circulation rather than reduced formation.     

Increased expression of the tetraspanins CD53 and CD63 on apoptotic human neutrophils

The recently discovered tetraspanin superfamily comprises a group of cell-surface proteins that are suggested to be involved in cell activation and signal transduction as well as in cell adhesion, motility, and metastasis. In this study, we have assessed the expression of two tetraspanins, CD53 and CD63, and two principal leukocyte adhesion molecules, CD11b and CD62L, on human apoptotic neutrophils. After aging of human neutrophils for 20 and 40 h in vitro, apoptosis was analyzed by light microscopy and flow cytometry. The binding of monoclonal antibodies directed against CD11b, CD62L, CD53, and CD63 on apoptotic and nonapoptotic cells was determined by dual-color flow cytometry. Aging of neutrophils in vitro resulted in a significant (P < 0.05) down-regulation of expression of the selectin CD62L, and a significantly increased expression of the two tetraspanins CD53 and CD63. The selective analysis of apoptotic versus nonapoptotic cells proved that both the increased expression of the tetraspanins and the loss of CD62L were restricted to the apoptotic subpopulation. An identical pattern of surface molecule expression was detected at 12 h after induction of apoptosis by an agonistic anti-Fas IgM monoclonal antibody. Further studies are required to clarify whether tetraspanins participate in the recognition of apoptotic circulating or extravasated neutrophils by macrophages.     

Systemic upregulation of leukocyte integrins in response to lower body ischemia-reperfusion during abdominal aortic aneurysm repair

Ischemia and reperfusion in myocardial infarction and stroke are associated with upregulation of leukocyte adhesion molecules, which contributes to tissue injury by facilitating leukocyte adhesion and infiltration in the affected tissues. Surgical repair of the abdominal aortic aneurysm involves clamping and declamping of the aorta, which necessarily results in ischemia and reperfusion of the lower half of the body. Given the large volume of the affected tissues and unimpeded venous return during reperfusion, we hypothesized that the procedure may result in upregulation of leukocyte integrins in the systemic circulation. To test this hypothesis, we studied neutrophil and monocyte surface densities of CD11b and CD18 in patients undergoing elective infrarenal abdominal aortic aneurysm repair. Serial blood samples were collected from the radial artery and femoral vein during the operation and leukocyte CD11b and CD18 surface densities were quantified by flow cytometry. Following reperfusion, CD11b expression in neutrophils and monocytes increased significantly in femoral venous and arterial blood. The mean time to peak expression of CD11 b in neutrophils and monocytes during reperfusion was 34.4 and 31.4 minutes in venous and 38.5 and 36.4 minutes in arterial blood, respectively. Similar rises in CD18 expression on neutrophils and monocytes were observed in venous and arterial blood. The mean time to peak expression of CD18 in neutrophils and monocytes during reperfusion was 34.0 and 40.0 minutes in venous and 47.5 and 50.0 minutes in arterial blood, respectively.