Humans with chronic psychological stress are prone to develop multiple disorders of body function including impairment of immune system. Chronic psychological stress has been reported to have negative effects on body immune system. However, the underlying mechanisms have not been clearly demonstrated. All immune cells are derived from hematopoietic stem cells (HSC) in the bone marrow, including myeloid cells which comprise the innate immunity as a pivotal component. In this study, to explore the effects of chronic psychological stress on HSC and myeloid cells, different repeated restraint sessions were applied, including long-term mild restraint in which mice were individually subjected to a 2 h restraint session twice daily (morning and afternoon/between 9:00 and 17:00) for 4 weeks, and short-term vigorous restraint in which mice were individually subjected to a 16 h restraint session (from 17:00 to 9:00 next day) for 5 days. At the end of restraint, mice were sacrificed and the total cell numbers in the bone marrow and peripheral blood were measured by cell counting. The proportions and absolute numbers of HSC (LinCD117Sca1CD150CD48) and myeloid cells (CD11bLy6C) were detected by fluorescence activated cell sorting (FACS) analysis. Proliferation of HSC was measured by BrdU incorporation assay. The results indicated that the absolute number of HSC was increased upon long-term mild restraint, but was decreased upon short-term vigorous restraint with impaired proliferation. Both long-term mild restraint and short-term vigorous restraint led to the accumulation of CD11bLy6C cells in the bone marrow as well as in the peripheral blood, as indicated by the absolute cell numbers. Taken together, long-term chronic stress led to increased ratio and absolute number of HSC in mice, while short-term stress had opposite effects, which suggests that stress-induced accumulation of CD11bLy6C myeloid cells might not result from increased number of HSC.
Animals ; Antigens, Ly ; metabolism ; Bone Marrow Cells ; cytology ; CD11b Antigen ; metabolism ; Cell Proliferation ; Hematopoietic Stem Cells ; cytology ; Mice ; Mice, Inbred C57BL ; Restraint, Physical ; Stress, Psychological

OBJECTIVETo 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.

METHODSFlow 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).

RESULTSThe 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).

CONCLUSIONCD11b/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.

Aged ; Arteriosclerosis Obliterans ; blood ; CD11b Antigen ; blood ; CD18 Antigens ; blood ; Cells, Cultured ; Drugs, Chinese Herbal ; pharmacology ; Female ; Humans ; Male ; Middle Aged ; Neutrophils ; cytology ; metabolism

OBJECTIVETo 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.

METHODSForty-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.

RESULTSThe 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).

CONCLUSIONExpression 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.

Aged ; CD11b Antigen ; biosynthesis ; blood ; CD18 Antigens ; biosynthesis ; blood ; Diabetes Mellitus, Type 2 ; blood ; drug therapy ; metabolism ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Humans ; Male ; Middle Aged ; Phytotherapy

OBJECTIVETo investigate the changes in perioperative expression level of CD11/CD18 of neutrophils in children undergoing cardiac surgery with cardiopulmonary bypass (CPB).

METHODSThirty 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.

RESULTIn 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).

CONCLUSIONCPB 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.

CD11b Antigen ; blood ; CD18 Antigens ; blood ; Cardiopulmonary Bypass ; Child, Preschool ; Enzyme-Linked Immunosorbent Assay ; Female ; Flow Cytometry ; Heart Defects, Congenital ; blood ; surgery ; Humans ; Infant ; Male ; Neutrophils ; cytology ; metabolism

OBJECTIVETo determine the effect of albumin administration on lung injury in traumatic/hemorrhagic shock (T/HS) rats.

METHODSForty-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.

RESULTSSignificant 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).

CONCLUSIONSThe infusion of albumin during resuscitation period can protect lungs from injury and decrease the expression of CD18/CD11b in T/HS rats.

Albumins ; therapeutic use ; Animals ; CD11b Antigen ; metabolism ; CD18 Antigens ; metabolism ; Disease Models, Animal ; Neutrophils ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Respiratory Distress Syndrome, Adult ; drug therapy ; etiology ; metabolism ; Shock, Hemorrhagic ; complications ; metabolism ; Treatment Outcome ; Wounds and Injuries ; complications ; metabolism

Glial cells play a critical role in morphine tolerance, resulting from repeated administration of morphine. Both the development and the expression of tolerance are suppressed by the analgesic lamotrigine. This study investigated the relationship between the ability of lamotrigine to maintain the antinociceptive effect of morphine during tolerance development and glial cell activation in the spinal cord. In a rat model, morphine (15 microg) was intrathecally injected once daily for 7 days to induce morphine tolerance. Lamotrigine (200 microg) was co-administered with morphine either for 7 days or the first or last 3 days of this 7 day period. Thermal nociception was measured. OX-42 and GFAP immunoreactivity, indicating spinal microglial and astrocytic activation were evaluated on day 8. Tolerance developed after 7 days of intrathecal morphine administration; however, this was completely blocked and reversed by co-administration of lamotrigine. When lamotrigine was coinjected with morphine on days 5-7, the morphine effect was partially restored. Glial cell activation increased with the development of morphine tolerance but was clearly inhibited in the presence of lamotrigine. These results suggest that, in association with the suppression of spinal glial cell activity, intrathecally coadministered lamotrigine attenuates antinociceptive tolerance to morphine.
Analgesics/*pharmacology ; Animals ; Antigens, CD11b/metabolism ; Astrocytes/cytology ; Drug Tolerance ; Immunohistochemistry ; Male ; Microglia/cytology ; Morphine/*pharmacology ; Nerve Tissue Proteins/metabolism ; Neuroglia/cytology/*metabolism ; Rats ; Rats, Sprague-Dawley ; Spinal Cord/*cytology ; Triazines/*pharmacology

The house dust mite (HDM) is considered to be the most common indoor allergen associated with bronchial asthma. In this study, we investigated whether crude extract of the HDM Dermatophagoides farinae could activate human eosinophilic leukemic cells (EoL-1) to induce upregulation of cell-surface adhesion molecules. When EoL-1 cells were incubated with D. farinae extract, expression of intercellular adhesion molecule-1 (ICAM-1) significantly increased on the cell surfaces compared to cells incubated with medium alone. In contrast, surface expression of CD11b and CD49d in EoL-1 cells was not affected by D. farinae extract. In addition, pretreatment of cells with NF- kappaB inhibitor (MG-132) or JNK inhibitor (SP600125) significantly inhibited ICAM-1 expression promoted by HDM extract. However, neither p38 MAP kinase inhibitor nor MEK inhibitor prevented HDM-induced ICAM-1 expression in EoL-1 cells. These results suggest that crude extract of D. farinae induces ICAM-1 expression in EoL-1 cells through signaling pathways involving both NF- kappaB and JNK.
Animals ; Anthracenes/pharmacology ; Antigens, CD11b/biosynthesis ; Cell Line, Tumor ; Cell Membrane/metabolism ; Eosinophils/*metabolism ; Flow Cytometry/methods ; *Gene Expression Regulation ; Humans ; Integrin alpha4/biosynthesis ; Intercellular Adhesion Molecule-1/*metabolism ; Leukemia/*metabolism ; Leupeptins/pharmacology ; Mitogen-Activated Protein Kinase 8/metabolism ; NF-kappa B/metabolism ; Pyroglyphidae ; p38 Mitogen-Activated Protein Kinases/metabolism

The possibility that P2X7 receptor (P2X7R) expression in microglia would mediate neuronal damage via reactive oxygen species (ROS) production was examined in the APPswe/PS1dE9 mouse model of Alzheimer's disease (AD). P2X7R was predominantly expressed in CD11b-immunopositive microglia from 3 months of age before Abeta plaque formation. In addition, gp91phox, a catalytic subunit of NADPH oxidase, and ethidium fluorescence were detected in P2X7R-positive microglial cells of animals at 6 months of age, indicating that P2X7R-positive microglia could produce ROS. Postsynaptic density 95-positive dendrites showed significant damage in regions positive for P2X7R in the cerebral cortex of 6 month-old mice. Taken together, up-regulation of P2X7R activation and ROS production in microglia are parallel with Abeta increase and correlate with synaptotoxicity in AD.
Aging ; *Alzheimer Disease/genetics/metabolism/pathology ; Amyloid beta-Peptides ; Animals ; Antigens, CD11b/immunology ; Blotting, Western ; Cerebral Cortex/metabolism/*pathology ; Disease Models, Animal ; Gene Expression ; Mice ; Mice, Transgenic ; Microglia/*metabolism/pathology ; Neurons/metabolism/*pathology ; Plaque, Amyloid ; Reactive Oxygen Species/*metabolism ; Receptors, Immunologic/analysis ; Receptors, Purinergic P2X7/*genetics/metabolism

OBJECTIVETo 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.

METHODSD 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.

RESULTIn 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.

CONCLUSIONThis 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.

6-Ketoprostaglandin F1 alpha ; blood ; Animals ; CD11b Antigen ; metabolism ; CD18 Antigens ; metabolism ; Carrageenan ; pharmacology ; Disease Models, Animal ; Endotoxins ; pharmacology ; Immunohistochemistry ; Interleukin-6 ; blood ; Leukocytes ; drug effects ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Thrombosis ; blood ; chemically induced ; metabolism ; pathology ; Tumor Necrosis Factor-alpha ; blood

OBJECTIVETo investigate whether phenylbutyrate (PB) combined with 5-aza-2'-deoxycytidine (5-Aza-CdR)could inhibit transcription repression and induce t(8;21) acute myelogenous leukemia (AML) Kasumi-1 cells to differentiate and undergo apoptosis.

METHODSKasumi-1 cells were treated with PB and 5-Aza-CdR at different concentrations in suspension culture. Cellular proliferation was determined by the MTT assay, expression of myeloid-specific differentiation antigen and cell cycles were analyzed by flow cytometry. Cell apoptosis were assessed using AnnexinV/PI staining and flow cytometry.

RESULTSTreatment of Kasumi-1 cells with PB caused a dose-dependent inhibition of proliferation, with an IC(50) of 2.3 mmol/L. When combined with 5-Aza-CdR, PB resulted in a greater growth inhibition with an IC(50) of 1.95 mmol/L. Treatment of Kasumi-1 cells with PB resulted in cell cycle arrest at G(0)/G(1), while combined treatment with PB and 5-Aza-CdR led to cell cycle arrest at G(2)/M. Expression of myeloid cell differentiation antigens CD11b and CD13 induced by PB was enhanced when Kasumi-1 cells were pretreated with low dose of 5-Aza-CdR. High, but not low, concentrations of 5-Aza-CdR could enhance early apoptosis of Kasumi-1 cells induced by PB.

CONCLUSIONPhenylbuty rate, when combined with 5-Aza-CdR, inhibits AML cell in vitro proliferation and increases apoptosis in a synergistic fashion.

Acute Disease ; Apoptosis ; drug effects ; Azacitidine ; administration & dosage ; analogs & derivatives ; pharmacology ; CD11b Antigen ; metabolism ; CD13 Antigens ; metabolism ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Dose-Response Relationship, Drug ; Drug Synergism ; Humans ; Leukemia, Myeloid ; immunology ; pathology ; Phenylbutyrates ; pharmacology