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

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 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

BACKGROUND/AIMS: For unknown reasons, caspase-1 -/- mice, protected against cisplatin-induced acute renal failure (ARF), are deficient in interleukin (IL)-1alpha. We thus asked whether IL-1alpha deficiency underlies the mechanism of protection against cisplatin-induced ARF in these mice. METHODS: Cisplatin (30 mg/kg) was injected intraperitoneally into wild-type C57BL/6 mice to produce a cisplatin-induced model of ARF. IL-1alpha was measured in control vehicle- and cisplatin-treated wild-type animals. We also examined whether IL-1alpha -/- mice were similarly protected against cisplatin-induced ARF. Additionally, infiltration of CD11b- and CD49b-positive cells, as markers of macrophages, natural killer, and natural killer T cells (pan-NK cells), was investigated in wild-type and IL-1alpha -/- mice. RESULTS: Compared with vehicle-treated mice, renal IL-1alpha increased in cisplatin-treated wild-type mice beginning on day 1. IL-1alpha -/- mice were shown to be protected against cisplatin-induced ARF. No significant difference in the infiltration of neutrophils or CD11b- and CD49b-positive cells were observed between wild-type and IL-1alpha -/- mice. CONCLUSIONS: Mice deficient in IL-1alpha are protected against cisplatin-induced ARF. The lack of IL-1alpha may explain, at least in part, the protection against cisplatin-induced ARF observed in caspase-1 -/- mice. Investigation of the protective mechanism (s) in IL-1alpha -/- mice in cisplatin-induced ARF merits further study.
Acute Kidney Injury/chemically induced/*immunology/pathology/physiopathology/prevention & control ; Animals ; Antigens, CD11b/analysis ; Apoptosis ; Biological Markers/blood ; Blood Urea Nitrogen ; *Cisplatin ; Creatinine/blood ; Disease Models, Animal ; Fluorescent Antibody Technique ; Integrin alpha2/analysis ; Interleukin-1alpha/deficiency/genetics/*metabolism ; Kidney/*immunology/pathology/physiopathology ; Killer Cells, Natural/immunology ; Macrophages/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Natural Killer T-Cells/immunology ; Necrosis ; Neutrophil Infiltration ; Time Factors

OBJECTIVETo 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.

METHODSSixty 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.

RESULTSThe 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).

CONCLUSIONKidney-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.

Aged ; Aged, 80 and over ; Aging ; drug effects ; CD11b Antigen ; blood ; CD18 Antigens ; blood ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Humans ; Kidney Diseases ; drug therapy ; metabolism ; Leukocytes ; metabolism ; Male ; Middle Aged ; Phytotherapy ; Proto-Oncogene Proteins c-bcl-2 ; blood ; bcl-2-Associated X Protein ; blood

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

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

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 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

To study the effects and possible mechanism of Vitamin K(2) (VK(2)) in the treatment of MDS-JSN04 cells, the changes of morphologic features of MDS-JSN04 cells were investigated by cytomorphology, the apoptosis of MDS-JSN04 cells was observed by transmission electron microscope; cellular proliferation was determined by the MTT assay; cell apoptosis, cell cycle shift and expression of myeloid-specific differentiation antigen (CD11b, CD13) were analyzed by flow cytometry (FCM). The expression of apoptosis-related genes bcl-2, survivin and bax were detected by retrotranscriptase polymerase chain reaction (RT-PCR); the activity of caspase-3 was determined by chemiluminescence assay. The results showed that the typical apoptotic morphological features appeared in cells treated with VK(2) for 72 hours; VK(2) induced apoptosis of MDS-JSN04 cells and in a dose-and-time-dependent manner, G(0)/G(1) cell arrest and significantly down-regulated the expression of bcl-2 and survivin, but had no effect on the expression of bax; the activity of caspase-3 significantly increased. It is concluded that VK(2) induces apoptosis of MDS-JSN04 cells through activating caspase-3 pathways and the apoptosis-related genes bcl-2, survivin may play an important role in this process.
Apoptosis ; drug effects ; CD11b Antigen ; analysis ; CD13 Antigens ; analysis ; Caspase 3 ; metabolism ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Flow Cytometry ; Gene Expression Regulation, Neoplastic ; Humans ; Inhibitor of Apoptosis Proteins ; Luminescent Measurements ; methods ; Microscopy, Electron, Transmission ; Microtubule-Associated Proteins ; genetics ; Myelodysplastic Syndromes ; genetics ; metabolism ; pathology ; Neoplasm Proteins ; genetics ; Proto-Oncogene Proteins c-bcl-2 ; genetics ; Reverse Transcriptase Polymerase Chain Reaction ; methods ; Vitamin K 2 ; pharmacology ; bcl-2-Associated X Protein ; genetics