Xuebijing Injection () and Resolvin D1 Synergize Regulate Leukocyte Adhesion and Improve Survival Rate in Mice with Sepsis-Induced Lung Injury / 中国结合医学杂志

<p><b>OBJECTIVE</b>To investigate the effect of combined application of Xuebijing Injection ( , XBJ) and resolvin D1 (RvD1) on survival rate and the underlying mechanisms in mice with sepsisinduced lung injury.</p><p><b>METHODS</b>The cecal ligation and puncture (CLP) method was used to develop a mouse sepsis model. Specific pathogen free male C57BL/6 mice were randomly divided into 5 groups (n=20 each): sham, CLP, CLP+XBJ, CLP+RvD1 and CLP+XBJ+RvD1. After surgery, mice in the CLP+XBJ, CLP+RvD1 and CLP+XBJ+RvD1 groups were given XBJ (25 μL/g body weight), RvD1 (10 ng/g body weight), and their combination (the same dose of XBJ and RvD1), respectively. In each group, 12 mice were used to observe 1-week survival rate, while the rest were executed at 12 h. Whole blood was collected for flow cytometric analysis of leukocyte adhesion molecules CD18, lung tissues were harvested for observing pathological changes, and testing the activity of myeloperoxidase (MPO) and the expression of intercellular cell adhesion molecule 1 (ICAM-1).</p><p><b>RESULTS</b>Compared with the CLP group, the histopathological damage of the lung tissues was mitigated, MPO activity was decreased in the CLP+XBJ and CLP+RvD1 groups (P<0.05). In addition, the 1-week survival rate was improved, proportion of CD18-expressing cells in whole blood and ICAM-1 protein expression in lung tissue were decreased in the CLP+XBJ+RvD1 group (P<0.05 or P<0.01).</p><p><b>CONCLUSIONS</b>XBJ together with RvD1 could effectively inhibit leukocyte adhesion, reduce lung injury, and improve the survival rate of mice with sepsis.</p>

Phenotypic and Functional Analysis of HL-60 Cells Used in Opsonophagocytic-Killing Assay for Streptococcus pneumoniae

Differentiated HL-60 is an effector cell widely used for the opsonophagocytic-killing assay (OPKA) to measure efficacy of pneumococcal vaccines. We investigated the correlation between phenotypic expression of immunoreceptors and phagocytic ability of HL-60 cells differentiated with N,N-dimethylformamide (DMF), all-trans retinoic acid (ATRA), or 1alpha, 25-dihydroxyvitamin D3 (VitD3) for 5 days. Phenotypic change was examined by flow cytometry with specific antibodies to CD11c, CD14, CD18, CD32, and CD64. Apoptosis was determined by flow cytometry using 7-aminoactinomycin D. Function was evaluated by a standard OPKA against serotype 19F and chemiluminescence-based respiratory burst assay. The expression of CD11c and CD14 gradually increased upon exposure to all three agents, while CD14 expression increased abruptly after VitD3. The expression of CD18, CD32, and CD64 increased during differentiation with all three agents. Apoptosis remained less than 10% until day 3 but increased after differentiation by DMF or ATRA. Differentiation with ATRA or VitD3 increased the respiratory burst after day 4. DMF differentiation showed a high OPKA titer at day 1 which sustained thereafter while ATRA or VitD3-differentiated cells gradually increased. Pearson analysis between the phenotypic changes and OPKA titers suggests that CD11c might be a useful differentiation marker for HL-60 cells for use in pneumococcal OPKA.

Phenotypic and Functional Analysis of HL-60 Cells Used in Opsonophagocytic-Killing Assay for Streptococcus pneumoniae

Differentiated HL-60 is an effector cell widely used for the opsonophagocytic-killing assay (OPKA) to measure efficacy of pneumococcal vaccines. We investigated the correlation between phenotypic expression of immunoreceptors and phagocytic ability of HL-60 cells differentiated with N,N-dimethylformamide (DMF), all-trans retinoic acid (ATRA), or 1alpha, 25-dihydroxyvitamin D3 (VitD3) for 5 days. Phenotypic change was examined by flow cytometry with specific antibodies to CD11c, CD14, CD18, CD32, and CD64. Apoptosis was determined by flow cytometry using 7-aminoactinomycin D. Function was evaluated by a standard OPKA against serotype 19F and chemiluminescence-based respiratory burst assay. The expression of CD11c and CD14 gradually increased upon exposure to all three agents, while CD14 expression increased abruptly after VitD3. The expression of CD18, CD32, and CD64 increased during differentiation with all three agents. Apoptosis remained less than 10% until day 3 but increased after differentiation by DMF or ATRA. Differentiation with ATRA or VitD3 increased the respiratory burst after day 4. DMF differentiation showed a high OPKA titer at day 1 which sustained thereafter while ATRA or VitD3-differentiated cells gradually increased. Pearson analysis between the phenotypic changes and OPKA titers suggests that CD11c might be a useful differentiation marker for HL-60 cells for use in pneumococcal OPKA.

A Rare Association Between Leukocyte Adhesion Deficiency Type I and Psoriasis in Humans

The beta2 integrins are expressed exclusively on leukocytes and participate in many immune and inflammatory processes. This subfamily comprises four heterodimeric glycoproteins with a common beta-subunit, designated beta2 (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 beta2 integrins in the etiopathogenesis of psoriasis.

Effect of Kidney-Tonifying and Blood-Promoting Recipe on the expression of CD11b/CD18 and Bcl-2/Bax in aged patients with kidney deficiency and blood stasis syndrome / 南方医科大学学报

<p><b>OBJECTIVE</b>To study the effect of Kidney-Tonifying plus Blood-Promoting Recipe on the expression of CD11b/CD18 and Bcl-2/Bax in elderly patients with kidney deficiency and blood stasis syndrome.</p><p><b>METHODS</b>Sixty elderly patients with kidney deficiency and blood stasis syndrome were randomized into two groups. Patients in the treatment group received Kidney-Tonifying plus Blood-Promoting Recipe, and those in the control group receive no treatment. The expression of CD11b/CD18, Bcl-2/Bax, D-Dimeride, CD62p, PAC-I and the rate of platelet aggregation in peripheral blood leukocytes before and after the treatment were examined using flow cytometry in both groups.</p><p><b>RESULTS</b>The Recipe significantly decreased the levels of CD11b/CD18, D-Dimeride, CD62p, PAC-I and the rate of platelet aggregation (P<0.01), and increased the levels of Bcl-2/Bax (P<0.01).</p><p><b>CONCLUSION</b>Kidney-Tonifying plus Blood-Promoting Recipe regulates CD11b/CD18 and Bcl-2/Bax expression in blood leukocytes and improves microcirculatory status, which can be one of the mechanisms underlying its therapeutic effect in elderly patients.</p>

A novel point mutation in CD18 causing leukocyte adhesion deficiency in a Chinese patient / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Leukocyte adhesion deficiency type 1 (LAD-1) is a rare, autosomal recessive inherited immunodeficiency disease characterized by recurrent severe bacterial infection, impaired pus formation, poor wound healing, associated with the mutation in the CD18 gene responsible for the ability of the leucocytes to migrate from the blood stream towards the site of inflammation. Correct and early diagnosis of LAD-1 is vital to the success of treatment and prevention of aggressive infections. The purpose of this study was to collect the clinical findings of the disease and to identify the genetic entity.</p><p><b>METHODS</b>CD18 expression in the peripheral blood leukocytes from the patient, his parents and normal control was measured with flow cytometry. The entire coding regions of the CD18 gene were screened with direct sequencing genomic DNA.</p><p><b>RESULTS</b>CD18 expression level on this patient's leukocyte surface was significantly decreased, with normal level in control group, his father and mother. Gene analysis revealed that this patient had a homozygous c.899A > T missense mutation in exon 8 of CD18 gene, causing the substitution of Asp to Val at the 300 amino acid. His parents were both heterozygous carriers while no such mutation was found in 50 normal controls.</p><p><b>CONCLUSION</b>This study disclosed a novel point mutation Asp 300 Val located in a highly conserved region (HCR) of CD18 and confirmed the heterogeneity of the mutations causing LAD-1, indicating it was quite beneficial to establish correct and early diagnosis in children with severe LAD-1.</p>

[Leukocyte adhesion deficiency]

Leukocyte adhesion deficiency [LAD] is a rare functional leukocyte disorder, which is divided into two separate types: LAD-1 and LAD-2. LAD-1 results from lack of beta2 integrin molecules [CD 11 and CD 18] on the leukocyte cell surface. These molecules are essential for leukocyte adhesion to endothelial cells and chemotaxis. The present case report is about a 42-month-old girl with recurrent otitis, pneumonia and gingivitis. On physical examination, patient was pale and malnourished. Multiple desquamated erythematous plagues were found on her body and extremities. Blood investigations revealed persistent leukocytosis with normal serum Immunoglobulin profile and complement. The diagnosis of LAD1 was made based on Flow cytometry finding; showing decreased in GD11 and CD 18 markers of PMN-a. When a patient has persistent leukocytosis and recurrent infections, investigation for the primary immune deficiency, specially leukocyte adhesion deficiency must be considered

Effects of WWOX on ovarian cancer cell attachment in vitro / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To observe the effects of WWOX on cell attachment in ovarian cancer, and to explore its mechanisms of action.</p><p><b>METHODS</b>Attachment assay was used to assess the adhesion of wwox-transfected PEO1 cells and vector-transfected PEO1 cells that were constructed, as well as PEO1 parent cells. Alpha/beta integrin-mediated cell adhesion assays were designed to identify cells surface integrins in PEO1 clone cells. Integrin function blocking experiments were designed to further determine integrins in PEO1 clone cells according to the integrin that was selected in integrin expression profiling. FACS analysis was used to further detect the level of integrin alpha3 on the cell membrane.</p><p><b>RESULTS</b>Attachment assay showed that adhesion of WWOX-transfected PEO1 cells to fibronectin was significantly slower than that in vector-transfected controls or PEO1 parent cells, cultured on the pre-coated fibronectin for 2 hours (P<0.01). The level of membranous integrins alpha2 and alpha3 in the WWOX-transfected PEO1 cells was significantly decreased, as compared with that in vector-transfected controls (P<0.05), but there was no association with the level of functioning integrins betal or beta2 in clone cells (P>0.05). The attachment assays were repeated after pre-incubating the cells with integrin alpha2 or alpha3 function-blocking antibodies. These results showed that blocking integrin alpha3 significantly reduced the binding to fibronectin of all the PEO1 clonal lines, as compared with cells pre-incubated with a non-specific IgG antibody (P<0.05). In contrast, preincubation with alpha2 blocking antibody had very little effect on fibronectin binding in these cells (P>0.05). FACS analysis showed that membranous integrin alpha3 expression revealed a marked reduction in WWOX-transfected cells than that in vector-transfected cells.</p><p><b>CONCLUSION</b>WWOX acts as an ovarian tumor suppressor by modulating the interaction between tumor cells and the extracellular matrix, decreasing integrin activity and adhesion of tumor cells to fibronectin. This suggests an important role for loss of WWOX tumor suppressor in promoting attachment and adhesion of ovarian cancer cells on locoregional peritoneum, and further resulting in enhancing locoregional peritoneal tumor spread.</p>

Anti-thrombosis effect and its mechanism of Qingkailing injection / 中国中药杂志

<p><b>OBJECTIVE</b>To investigate the anti-thrombosis effect and its mechanism of Qingkailing injection (QKL).</p><p><b>METHOD</b>SD rats were randomly divided into control group, model group and QKL 2.5, 5.0, 10 groups. QKL were given (i.p.) to rats once a day for successively 4 days. The rats in all groups but control were pretreated with carrageenin (Ca) i.p. at 16 h before the last dose of QKL and followed by intravenous injection of endotoxin ( LPS fom E. coli O111:B4) 50 microg x kg(-1) 30 min after the last dosing of QKL. Thrombosis in rat tails were observed at 24 h after injection of LPS. The number of white blood cells and platelets, serum TNF-alpha, IL-6 level, CD11b/CD18 expression of white blood cells and platelet aggregation were analysed.</p><p><b>RESULT</b>QKL obviously inhibited the LPS/Ca-induced thrombosis as showed a reduced infarction range due to thrombosis in tails. The sera concentration of TNF-alpha and IL-6, expression of CD11b/CD18 in WBC and platelet coagulation rate were reduced after QKL treatment.</p><p><b>CONCLUSION</b>The anti-thrombosis action of QKL is associated with inhibition of WBC activation and adherence, reduction of inflammatory factor release and abating of platelet coagulation rate. The anti-thrombosis mechanism of QKL is consistent with its function of clearing away heat-evil and toxic materials.</p>

Development of virulent heat-evil-induced thrombosis animal model / 中国中药杂志

<p><b>OBJECTIVE</b>To develop a virulent heat-evil-induced thrombosis animal model, and provide a rational animal model for pathogeny and pathogenesis research of thrombosis-related diseases, anti-thrombosis activity screening and pre-clinical studies of CAHT formula.</p><p><b>METHOD</b>SD rats were pretreated with carrageenin (Ca) intraperitoneal injection, followed by intravenous injection of endotoxin (LPS from E. coli O111:B4) 50 microg x kg(-1) 16 h later. Thrombosis in rat tails were observed during 12-24 h after injection of LPS. The inflammatory mechanism of this model were investigated by analyzing serum level of TNF-alpha, IL-6, TXB2 and 6-keto-PGF 1alpha, CD11b/CD18 expression of white blood cells (WBC) and P-selectin expression of vessel walls.</p><p><b>RESULT</b>In LPS/Ca model group, thrombosis can be clearly observed in the distal part of rat tails after 12-24 h of LPS/Ca treatment. High level of TNF-alpha and IL-6 can be measured in serum. The expression of CD11b/CD18 in WBC and P-selectin in vessel endothelium significantly increased and the number of WBC in peripheral blood markedly decreased shortly after LPS/Ca treatment. The adherence of white blood cells to vessel endothelium which can be seen by microscope mainly contributed to the decrease of WBC. The results indicated that there was obvious inflammation after treatment with LPS/Ca, suggesting that inflammation was the key mechanism for this model.</p><p><b>CONCLUSION</b>This model was developed through treatment of LPS in combination with Ca, of which LPS is considered to be an exotic virulent heat-evil in TCM, while the inflammatory molecules produced in this model, such as TNF-alpha, IL-6, CD11b/CD18 and P-selectin belong to internal virulent heat-evils, so this animal model consists of pathogeny and pathogenesis of virulent heat-evils. virulent heat-evil.</p>

[Leukocyte adhesion deficiency syndrome and report of three cases]

Leukocyte adhesion deficiency syndrome [LADS] is a rare inherited immunodeficiency in which the frunction of leukocytes, particularly the phagocytes are disturbed. In the present study, we report three cases with LADS [2 male infants and 1 female child] who had a history of delay in separation of umbilical cord. One infant admitted for skin infection and two patients admitted in hospital following bacterial and fungal infections in nose and finger. All cases had a remarkable leukocytosis, neutrophilia and decreased of CD 11 and CD 18. LADS is a congenital syndrome causes recurrent bacterial and fungal infections. Usually all patients have a history of delayed separation of umbilical cord

Effect of cardiopulmonary bypass on CD11/CD18 expression of neutrophils in children undergoing cardiac surgery / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the changes in perioperative expression level of CD11/CD18 of neutrophils in children undergoing cardiac surgery with cardiopulmonary bypass (CPB).</p><p><b>METHODS</b>Thirty children patients with congenital heart disease underwent cardiac surgery with CPB (CPB group) and the control group consisted of 20 children who received thoracic or general surgery without CPB. Blood samples were drawn at the following time points: pre-surgery, 15 min after onset of CPB, immediately after CPB, 2 h after surgery and on the 1st, 2nd, 3rd postoperative day. D11/CD18 expression on neutrophils and serum concentration of IL-6 and IL-8 were analyzed by flow cytometry and enzyme-linked immunosorbent assay, respectively.</p><p><b>RESULT</b>In CPB group plasma levels of IL-6 and IL-8 increased significantly and peaked at 2 h after initiation of CPB (P<0.05), and descended to the after-anesthesia level at 3rd day after operation. In non-CPB group there was a similar trend of changes in IL-6 and IL-8, but to a much lesser extent. The level of CD11b/CD18 in CPB group began to increase significantly and peaked at 15 min after initiation of CPB (P <0.05), and descended to the after-anesthesia level at 2 h after operation. There was no significant changes of CD11b/CD18 in control group (P >0.05). No significant differences were detected at any time points with respect to expression of CD11a/CD18 and CD11c/CD18 in both groups (P >0.05).</p><p><b>CONCLUSION</b>CPB surgery of children can cause increasing of the CD11b/CD18 expression level of neutrophil but has no significant effect on CD11a/CD18 and CD11c/CD18. CD11b/CD18 may play an important role in the systemic inflammation induced by CPB.</p>

Protective effect of tanshinone II A on lipopolysaccharide-induced lung injury in rats / 中国结合医学杂志

<p><b>OBJECTIVE</b>To explore the protective effect of tanshinone II A on lipopolysaccharide (LPS)-induced lung injury in rats, and possible mechanism.</p><p><b>METHODS</b>LPS (O(111): B4) was used to produce a rat model of acute lung injury. Sprague-Dawley rats were randomly divided into 3 groups (8 in each group): the control group, the model group (ALI group), and the tanshinone II A treatment group. Expression of adhesion molecule CD18 on the surface of polymorphonuclear neutrophil (PMNCD18) in venous white blood cells (WBC), and changes in coagulation-anticoagulant indexes were measured 6 h after injection of LPS or normal saline. Changes in malondialdehyde (MDA) content, wet and dry weight (W/D) ratio and morphometry of pulmonary tissue as well as PMN sequestration in the lung were also measured.</p><p><b>RESULTS</b>(1) When compared with the control group, expression of PMNCD18 and MDA content were enhanced in the ALI group with a hypercoagulable state (all P<0.01) and an increased W/D ratio (P<0.05). Histopathological morphometry in the lung tissue showed higher PMN sequestration, wider alveolar septa; and lower alveolar volume density (V(V)) and alveolar surface density (S(V)), showing significant difference (P<0.01). (2) When compared with the ALI group, the expression of PMN-CD18, MDA content, and W/D ratio were all lower in Tanshinone II A treatment group (P<0.05) with ameliorated coagulation abnormality (P<0.01). Histopathological morphometry in the lung tissue showed a decrease in the PMN sequestration and the width of alveolar septa (both P<0.01), and an increase in the V(V) and S(V) (P<0.05, P<0.01).</p><p><b>CONCLUSION</b>Tan II A plays a protective role in LPS-induced lung injury in rats through improving hypercoagulating state, decreasing PMN-CD18 expression and alleviating migration, reducing lipid peroxidation and alleviating pathological changes.</p>

Expression of leukocyte adhesion molecular MAC-1 [CD11B/CD18] and L-selectin[CD62L] in patients with chronic renal failure undergoing regular hemodialysis

Mac1 and L-selectin expressed on leukocytes are critical for leukocyte adhesion to inflammed endothelium. Degranulation of polymorphnuclear leukocytes [PMN] during hemodialysis [HD] is usually assessed by measuring degranulation products. Our aim was to evaluate the effect of HD on leukocyte activation and degranulation. Fifteen normal controls and fifteen patients under chronic renal dialysis treatment were studied for Mac 1 and L-selectin expression on granulocytes by flowcytometry. PMN degranulation products; myeloperoxidase[MPO] and lactoferrin[LF] were determined in serum by ELISA method. The results of Mac 1 expression on granulocytes demonstrated a statistical significant increase in post HD compared to both pre HD [P<0.05] and control groups [P<0.05]. A statistical significant increase was also noted between Pre HD and the control group [P<0.05]. Post HD results showed a statistical significant decreased L-selectin granulocyte expression when compared to Pre HD group [P<0.05]. Post HD group showed a statistically significant increase of both MPO and LF when compared to predialysis and control group [P<0.05]. There was also a statistically significant increase in Pre HD group compared to control group in both MPO and LF levels [P<0.05].In post hemodialysis group there was a negative correlation between MAC1 and L-selectin [r=0.41]. Our finding showed that HD might influence the expression of leukocyte adhesion molecules and subsequently degranulation of PMN. Their measurement might be an indicator of PMN disturbed functions

Intervention of xuefu zhuyu oral liquid on expression of adhesion molecule CDllb/CD18 in neutrophils in patients with ateriosclerosis obliterans / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To observe the expression of adhesion molecular CD11b/CD18 in peripheral neutrophils and its relation with arteriosclerotic obliterans (ASO), and to study the effect of Xuefu Zhuyu Oral Liquid (XZOL) on it.</p><p><b>METHODS</b>Flow cytometery analysis was used to detect the expression of CD11b/CD18 in peripheral neutrophils of 30 patients with ASO and 30 healthy subjects by direct immunofluroscent technique. Neutrophils were separated from whole blood of ASO patients and cultured, CD11b/CD18 were detected after the cultured cells were interfered with XZOL dilution at different time points (1h,6h,12h).</p><p><b>RESULTS</b>The expression of CD11b/CD18 in neutrophils in ASO patients was significantly higher than that in the healthy subjects (P < 0.05) and stepped in keeping with the severity of the disease. It was significantly lowered in the treated group 6 and 12 h after XZOL intervention, showing significant difference as compared with that in the control group and the level 1 h after medication (P < 0.05).</p><p><b>CONCLUSION</b>CD11b/CD18 may involve in the pathogenesis of ASO and be related to the severity of arteriosclerosis. The possible mechanism of XZOL in treating and preventing ASO might be through reducing the expression of CD11b/CD18 in peripheral neutrophils to interfere the adhesive function of them.</p>

Signaling transduction pathways involved in basophil adhesion and histamine release / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Little is known about basophil with respect to the different signaling transduction pathways involved in spontaneous, cytokine or anti-IgE induced adhesion and how this compares to IgE-dependent and IgE-independent mediator secretion. The purpose of the present study was to investigate the roles of beta1 and beta2 integrins in basophil adhesion as well as hosphatidylinositol 3-kinase (PI3K), src-kinases and extracellular signal regulated kinase (ERK) 1/2 in basophil adhesion and histamine release (HR).</p><p><b>METHODS</b>Basophils (purity of 10% - 50%) were preincubated with anti-CD29 or anti-CD18 blocking antibodies before used for adhesion study. Basophils were preincubated with the pharmacological inhibitors wortmannin, PP1, PD98059 before used for adhesion and HR study. Cell adherence to bovine serum albumin (BSA) or fibronectin (Fn) was monitored using cell associated histamine as a basophil marker and the histamine was measured by the glass fiber assay.</p><p><b>RESULTS</b>Basophil spontaneous adhesion to Fn was inhibited by anti-CD29. Interleukin (IL)-3, granulocyte/macrophage colony stimulating factor (GM-CSF) induced adhesion to BSA was inhibited by anti-CD18. Wortmannin at 1 micromol/L and PP1 at 20 micromol/L strongly interfered with, whereas PD98059 at 50 micromol/L weakly inhibited basophil spontaneous adhesion to Fn. One micromol/L wortmannin strongly inhibited IL-3, IL-5, GM-CSF and anti-IgE induced adhesion to BSA. PP1 at 20 micromol/L partly inhibited anti-IgE induced adhesion. Fifty micromol/L PD98059 marginally inhibited IL-5, weakly inhibited anti-IgE, partly inhibited GM-CSF induced adhesion. Wortmannin, PP1 and PD98059 inhibited anti-IgE (1:100 or 1:1000) induced basophil HR in a dose dependent manner. They inhibited calcium ionophore A23187 (10 micromol/L, 5 micromol/L) induced basophil HR in a dose dependent manner, but to different extend with PP1 being the most efficient.</p><p><b>CONCLUSIONS</b>Basophil spontaneous adhesion to Fn is mediated by beta1-integrins whereas cytokine induced adhesion to BSA is mediated by beta2-integrins. PI3K, src-kinases and ERK1/2 play distinct signaling roles in basophil adhesion and HR. PI3K is the key player while ERK1/2 is the weakest participant.</p>

Protective effect of albumin on lungs injury in traumatic/hemorrhagic shock rats / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To determine the effect of albumin administration on lung injury in traumatic/hemorrhagic shock (T/HS) rats.</p><p><b>METHODS</b>Forty-eight adult Sprague-Dawley rats were divided into three groups randomly (n=16 in each group): Group A, Group B, Group C. In Group A, rats underwent laparotomy without shock. In Group B, rats undergoing T/HS were resuscitated with their blood plus lactated Ringer's (twice the volume of shed blood). In Group C, rats undergoing T/HS were resuscitated with their shed blood plus additional 3 ml of 5% human albumin. The expression of polymorphonuclear neutrophils CD18/CD11b in jugular vein blood was evaluated. The main lung injury indexes (the activity of myeloperoxidase and lung injury score) were measured.</p><p><b>RESULTS</b>Significant differences of the expression of CD18/11b and the severity degree of lung injury were founded between the three groups. (P<0.05). The expression of CD18/CD11b and the main lung injury indexes in Group B and Group C increased significantly compared with those in Group A (P<0.05). At the same time, the expression of CD18/CD11b and the main lung injury indexes in Group C decreased dramatically, compared those in Group B (P<0.05).</p><p><b>CONCLUSIONS</b>The infusion of albumin during resuscitation period can protect lungs from injury and decrease the expression of CD18/CD11b in T/HS rats.</p>

Differential expression of a homing-related molecule repertoire among umbilical cord blood, mobilized peripheral blood and bone marrow-derived hematopoietic stem/progenitor cells / 中华血液学杂志

<p><b>OBJECTIVE</b>To compare the expression profiles of a set of homing-related molecules (HRM) repertoire expressed on hematopoietic stem/progenitor cells (HS/PC) from different sources.</p><p><b>METHOD</b>The expression levels of HRM on HS/PC from umbilical cord blood (UCB), mobilized peripheral blood (mPB) and bone marrow (BM) were assessed using a highly sensitive 4-color flow cytometric analysis.</p><p><b>RESULTS</b>UCB-derived CD34(bright) cells, as well as mPB- and BM-derived CD34(bright) cells strongly expressed CD44, CD11a, CD18, CD62L, CD31 and CD49d. On the other hand, significantly lower expressions of CD49e, CD49f, CXCR-4 and CD54 on UCB-derived CD34(bright) and CD34(bright)CD38(-) cells, compared with those on mPB- and BM-derived CD34(bright) and CD34(bright)CD38(-) cells, were observed. None of UCB-, mPB- and BM-derived CD34(bright) cells expressed other chemokine receptors, including CCR-1, CCR-2, CCR-3, CCR-5, CXCR-1, CXCR-2, CXCR-3 and CXCR-5. Another striking finding was that only mPB-derived CD34(bright) cells expressed significant levels of both the matrix metalloproteinases MMP-2 \[(11.4 +/- 4.9)%\] and MMP-9 \[(27.6 +/- 7.8)%\].</p><p><b>CONCLUSION</b>HS/PC from UCB have some defects of expression of HRM repertoire, which might partly explain the cause(s) of delayed hematopoietic reconstitution after UCB transplant.</p>

Effect of esculentoside A on cellular adhesion / 药学学报

<p><b>AIM</b>To investigate the anti-inflammatory mechanism of esculentoside A (EsA) and to observe the effects of EsA on cellular adhesion between human umbilical vein endothelial cell (VEC304) and human neutrophil and to further observe the mRNA expression of intercellular adhesion molecule-1 (ICAM-1) and cluster of differentiation 18(CD18).</p><p><b>METHODS</b>The hemocyte counting method was used for assaying the adhesion rate between VEC304 and neutrophil. The RT-PCR method was used for measuring the mRNA expression of ICAM-1 and CD18.</p><p><b>RESULTS</b>The adhesion rate between VEC304 and neutrophil was increased with treatment of lipopolysaccharide(LPS). EsA (3 - 12 x 10(-6) mumol.L-1) was shown to inhibit the high cellular adhesion induced by LPS. A further investigation of adhesion molecules mRNA expression was undertaken using semi-quantitative reverse transcribed polymerase chain reaction (RT-PCR). The results of RT-PCR from VEC304 and human neutrophil treating with LPS showed that ICAM-1 and CD18 mRNA expressions were higher than those of normal cells, while this increased expression of ICAM-1 and CD18 mRNA was remarkably attenuated by the addition of EsA.</p><p><b>CONCLUSION</b>EsA was found to inhibit the increased adhesion rate induced by LPS. Moreover, LPS induced high expression of ICAM-1 and CD18 was inhibited with treatment of EsA. It might be involved in the mechanisms of anti-inflammation of EsA.</p>

Effect of Chinese herbal medicine for activating blood circulation to remove stasis on CD11b/CD18 expression in patients with diabetes mellitus type 2 / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To explore the expression of polymorphonuclear leucocyte adhesive molecules CD11b/CD18 and to study the possible mechanism of Chinese herbal medicine (TCM) for activating blood circulation to remove stasis in preventing vascular diseases.</p><p><b>METHODS</b>Forty-nine patients with diabetes mellitus (DM) but with no complications of hypertension and nephropathy were randomly divided into the treated group (26 patients treated by TCM) and the control group (23 patients treated by conventional treatment). They were treated for 3 months. The changes of urinary albumin excretion rate (UAER), CD11b/CD18 expression and tumor necrosis factor-alpha (TNF-alpha) concentration before and after treatment were observed.</p><p><b>RESULTS</b>The CD11b/CD18 expression and TNF-alpha concentration in DM patients were higher than those of normal range (P < 0.01). After treatment, the UAER, CD11b/CD18 expression and TNF-alpha concentration lowered significantly in the treated group (P < 0.01), but unchanged in the control group. Correlation analysis showed that the lowering of UAER was positively correlated with decreasing of CD11b/CD18 (r = 0.64, P < 0.01) and TNF-alpha (r = 0.56, P < 0.01).</p><p><b>CONCLUSION</b>Expression of CD11b/CD18 increases in patients with DM type 2. The mechanism of Chinese herbal medicine for activating blood circulation to remove stasis in preventing vascular disease in possibly related with its effect in inhibiting CD11b/CD18 expression.</p>