Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P10145 (IL-8)
 23,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the role of T cells in diffuse panbronchiolitis (DPB), we investigated T-cell subsets in bronchoalveolar lavage fluid (BALF) or 33 patients with DPB, nine patients with bronchiectasis, and 20 healthy volunteers. BALF from DPB patients contained a higher percentage of neutrophils than that from patients with bronchiectasis or healthy volunteers, whereas the percentage of lymphocytes was similar in the three groups. DPB patients, however, had a higher number of lymphocytes and a reduced CD4/CD8 ratio compared with the other subjects. A two-color analysis of T-cell subsets in peripheral blood and BALF revealed a significant increase in the percentage and number of CD8+HLA-DR+ cells and in the number of CD4+HLA-DR+ cells in BALF of DPB patients. The expression of the adhesion molecules CD 11a and CD18 on lung CD3+ cells was enhanced over that on blood CD3+ cells in DPB patients. However, there was no significant difference in the expression of these antigens in peripheral blood or BALF among the groups. There was no significant relationship between BALF interleukin (IL)-8 and lymphocyte accumulation in the lungs of the DPB patients, whereas a significant correlation between the percentage of neutrophils and IL-8 levels in BALF of DPB patients was observed. After treatment with macrolide antibiotics, a significant reduction in the number of lymphocytes and activated CD8+ cells and an elevation in the CD4/CD8 ratio in BALF of DPB patients was observed. Our findings suggest an activation of CD8+ cells in the airway lumen of DPB patients, supporting the hypothesis that lymphocytes are important cellular components of bronchial inflammation in DPB.
 ...
PMID:Increase in activated CD8+ cells in bronchoalveolar lavage fluid in patients with diffuse panbronchiolitis. 763 15

Children undergoing cardiopulmonary bypass (CPB) surgery for congenital heart defects develop an acute post-operative capillary leak which may be due to endothelial injury inflicted by adherent neutrophils (PMN). Direct immunofluorescence and flow cytometry were used to measure CD11a/CD18, CD11b/CD18 and L-selectin (L-s) expression on circulating PMN in CPB circuits containing human blood and in children undergoing CPB. In vitro, a general rise in CD11b/CD18 expression over 2 h contrasted with complete loss of L-s in a small but progressively increasing proportion of PMN. Marked but inconsistent changes in CD11b/CD18 and L-s were observed in vivo, in conjunction with fluctuations in circulating PMN count. Circulating IL-8 was detected starting at rewarming from hypothermia and reperfusion of the heart and lungs with a simultaneous, closely correlated rise in both PMN count and circulating elastase. IL-1 and TNF were not detected. These studies demonstrate changes in the pathways of PMN-endothelial interaction during and after CPB.
 ...
PMID:Changes in neutrophil CD11b/CD18 and L-selectin expression and release of interleukin 8 and elastase in paediatric cardiopulmonary bypass. 768 23

Interleukin-2 (IL-2)-dependent large granular lymphocytes (LGL) with a distinctive surface phenotype were generated from histologically normal duodenal biopsy tissues. Immunoperoxidase staining of the mucosa with an anti-CD56 monoclonal antibody revealed LGL localized in the lamina propria rather than in the epithelium. Light and electron microscopy demonstrated azurophilic and electron-dense cytoplasmic granules. Flow cytometry analysis revealed that these cells express CD45, CD56, CD2, CD7, CD11a, CD18, CD69 and the intermediate affinity (p70) IL-2 receptor (IL-2R) but not CD57, CD16, CD3, CD4, CD5, CD8, CD45RA, CD25, or the high affinity p55 IL-2R. The LGL proliferated when cultured in the presence of human rIL-2 but not in the presence of human rIL-4. Functional studies demonstrated that the LGL had strong cytotoxicity against natural killer (NK) target cells, K562, but not NK-resistant targets such as Colo 205, Melanoma and Epstein-Barr virus (EBV)-transformed B-cell lines. The LGL expressed genes for IL-5, IL-8, granulocyte-macrophage colony-stimulating factor (GM-CSF) and tumour necrosis factor-alpha (TNF-alpha) and the corresponding cytokines were detected in culture supernatant. These results provide evidence for an important role of gut mucosal LGL in the induction and regulation of inflammation and immunity in the gut.
 ...
PMID:Morphological, phenotypic and functional characteristics of a pure population of CD56+ CD16- CD3- large granular lymphocytes generated from human duodenal mucosa. 769 28

To evaluate the inflammatory response to the cardiopulmonary bypass, we investigated the serum levels of tumor necrosis factor alpha (TNF alpha), interleukin 8 (IL-8), and the expression of leukocyte adhesion molecule CD18. Six patients who underwent elective coronary artery bypass grafting were studied. TNF alpha was elevated significantly 30 minutes after the start of CPB and returned to the baseline 60 minutes after CPB. IL-8 increased significantly after the start of CPB and reached a peak at 10 minutes after release of the aortic cross-clamp, remaining significantly elevated until 10 minutes after the end of CPB (P < 0.05). Circulating neutrophil count and granulocyte elastase increased significantly 10 minutes after release of the aortic-cross clamp and remained high until the first postoperative day. The increase of the neutrophil CD18 expression was not observed. This study demonstrates elevated TNF alpha and IL-8 levels during CPB followed by increases of the neutrophil and the granulocyte elastase, which may be of importance in the systemic inflammatory response to CPB, especially in the development of postperfusion lung injury.
 ...
PMID:[Responses of TNF alpha, IL-8, and leukocyte adhesion molecule CD18 to cardiopulmonary bypass]. 769 21

Recent studies suggest that interleukin (IL)-8 exerts a direct influence on several functions such as the chemotaxis or proliferation of human keratinocytes (HK). Since the effects of IL-8 in skin are mediated through specific receptors, we have studied the characteristics of the keratinocyte IL-8 receptor. We could identify specific binding sites for IL-8 in cultured HKs by flow cytometry. Pretreatment of the cells with tumor necrosis factor (TNF)-alpha or IL-1 alpha resulted in a significant increase in IL-8 binding. IL-8 selectively induced expression of HLA-DR antigen, but had no effect on the expression of other cell surface antigens (CD11a, CD18, CD36 and CD54).
 ...
PMID:Interleukin-8 induces HLA-DR expression on cultured human keratinocytes via specific receptors. 771 52

Monocytes and polymorphonuclear leukocytes (PMNLs) migrate across cytokine (interleukin-1, tumor necrosis factor) activated endothelium or unstimulated endothelium in response to chemotactic factors in vitro and in vivo utilizing the CD11/CD18 (i.e., beta 2 integrin) adhesion molecule complex. However, in vivo studies have suggested that under some conditions and/or in certain tissues, leukocyte migration can also proceed via CD11/CD18-independent mechanisms. Here we compared adhesion mechanisms involved in the migration of 51Cr-labeled blood monocytes and PMNLs across human umbilical vein endothelium (HUVE) monolayers. We observed that monocyte transendothelial migration was not inhibited by monoclonal antibody (mAb) to CD18, when the HUVE was activated with IL-1 and the chemotactic factor C5a induced the migration. This CD18-independent monocyte migration was blocked by treatment of the monocyte with mAb to beta 1 or alpha 4 integrin, suggesting that very late activation antigen 4 (VLA-4) on the monocyte served as the alternative migration mechanism. In contrast to monocytes, mAb to CD18 inhibited PMNL migration to C5a across IL-1-activated HUVE, but only by 66%, significantly less than with C5a alone (84%) or IL-1-activated HUVE alone (95%). The migration of anti-CD18 mAb-treated PMNLs was not inhibited by function-blocking mAbs to sialyl Lewisx, L-selectin, beta 1 or alpha 4 integrin, the beta 3-related leukocyte response integrin, IL-8, or platelet-activating factor (PAF) antagonists, alone or in combination. Antibody-blocking studies of the ligands on HUVE indicated that E-selectin may be partially involved in this CD18-independent PMNL migration but that ICAM-1, VCAM-1, PECAM-1, and P-selectin are not involved. Of several chemotactic factors tested, C5a and C5adesArg in activated plasma were the most active in inducing CD18-independent migration of PMNLs across IL-1-activated HUVE. These results demonstrate that (1) monocytes can utilize VLA-4 for optimal transendothelial migration and (2) PMNLs may have a novel CD18-independent migration mechanism that is activated by C5a in conjunction with one or more ligands on cytokine-activated endothelium. This may involve, in part, E-selectin interacting with a yet to be identified counterreceptor on PMNLs.
 ...
PMID:CD11/CD18-independent transendothelial migration of human polymorphonuclear leukocytes and monocytes: involvement of distinct and unique mechanisms. 772 14

Inflammation is a primary pathological process. The development of an inflammatory reaction involves the movement of white blood cells through the endothelial lining of blood vessels into tissues. This process of transendothelial cell migration of neutrophils has been shown to involve neutrophil beta 2 integrins (CD18) and endothelial cell platelet-endothelium cell adhesion molecules (PECAM-1; CD31). We now show that F(ab')2 fragments of the monoclonal antibody B6H12 against integrin-associated protein (IAP) blocks the transendothelial migration of neutrophils stimulated by an exogenous gradient of the chemokine interleukin 8 (IL-8; 60% inhibition), by the chemotactic peptide N-formyl-methionylleucylphenylalanine (FMLP; 76% inhibition), or by the activation of the endothelium by the cytokine tumor necrosis factor alpha (98% inhibition). The antibody has two mechanisms of action: on neutrophils it prevents the chemotactic response to IL-8 and FMLP, and on endothelium it prevents an unknown but IL-8-independent process. Blocking antibodies to IAP do not alter the expression of adhesion proteins or production of IL-8 by endothelial cells, and thus the inhibition of neutrophil transendothelial migration is selective. These data implicate IAP as the third molecule essential for neutrophil migration through endothelium into sites of inflammation.
 ...
PMID:Transendothelial migration of neutrophils involves integrin-associated protein (CD47). 773 16

Optical microscopy and image processing have been employed to study the distribution of several cell surface receptors on living human neutrophils during opsonin-dependent and opsonin-independent phagocytosis. Receptors were labeled using fluorescein-, rhodamine-, or AMCA-conjugated F(ab')2 fragments of anti-Fc gamma RIIIB (CD16), anti-CR3 (CD11b/CD18), and anti-uPAR (urokinase-type plasminogen activator receptor) antibodies, intact phycoerythrin-labeled interleukin 8, and fluorescein- or rhodamine-labeled Con A (concanavalin A), Boc-PLPLP (tert-butyl-oxycarbonyl-Phe(D)-Leu-Phe(D)-Leu-Phe-OH), and N-formyl-Nle-Leu-Phe-Nle-Tyr-Lys. Labeled neutrophils were observed during the phagocytosis of IgG-opsonized erythrocytes and nonopsonized latex beads, Escherichia coli, and Staphylococcus aureus. To quantitate receptor distribution, cells were divided into four quadrants with the first being the point of attachment and the fourth being opposite the point of attachment. Ligated formyl peptide receptors, and to a lesser extent CR3, accumulated at the sites of target internalization for all forms of phagocytosis examined. However, Fc gamma RIIIB, uPAR, IL-8, Con A, and the FPR antagonist FBoc-PLPLP were not polarized on cells during phagocytosis. These data suggest that agonist-labeled formyl peptide receptors may play a broader role in leukocyte function than previously suggested, including possible participation in phagocytosis.
 ...
PMID:Imaging the spatial distribution of membrane receptors during neutrophil phagocytosis. 773 43

Cells infiltrating the nonsensory epithelium of the vomeronasal organ of virus-antibody-free rats exhibited surface immunoreactivity for beta 2-microglobulin and immunoglobulin (Ig) E. They were further characterized by using immunohistochemical techniques with antibodies to cell-specific markers or histochemical techniques for immunocytes with surface receptors for IgE. Localization of intracellular granules immunoreactive for lactoferrin and CD18, a leukocyte adhesion molecule, unequivocally identified these cells as neutrophils. The low number of IgA- and IgG-immunoreactive B lymphocytes, T lymphocytes, and accessory immunocytes in the vomeronasal organ as well as the rest of the nasal cavity confirmed the absence of infection. We hypothesize that the operation of the vomeronasal pump induces repeated episodes of transient focal ischemia followed by reperfusion, which results in release of neutrophil chemoattractants and modulation of adhesion factors that regulate the extravasation and migration of neutrophils into the nonsensory epithelium. The distribution of immunoreactivity for interleukin 8 suggests that it is not the primary neutrophil chemoattractant in this system while that of CD18 suggests its active involvement in neutrophil extravasation. In addition to their role in immune surveillance, neutrophils may stimulate ion/water secretion into the vomeronasal lumen, affecting the perireceptor processes regulating stimulus access and clearance from the sensory epithelium.
 ...
PMID:Identification of neutrophils in the nonsensory epithelium of the vomeronasal organ in virus-antibody-free rats. 775 Jan 29

Molecules representative of different classes of chemotactic agents, including formyl-Met-Leu-Phe (FMLP), C5a, leukotriene B4, platelet-activating factor, and interleukin (IL)-8, caused a rapid reduction in the IL-1 binding capacity by human polymorphonuclear leukocytes (PMN), a cell type expressing predominantly the IL-1 type II decoy receptor (IL-1 decoy RII). N-t-Boc-Met-Leu-Phe, an antagonist for the FMLP receptor, inhibited the loss of IL-1 binding capacity induced by FMLP. Monocyte chemotactic protein 1, a chemokine related to IL-8 but inactive on PMN, had no effect on IL-1 binding in this cell type. FMLP was selected for further detailed analysis of chemoattractant-induced loss of IL-1 binding by PMN. The action of FMLP was rapid, reaching 50% of its maximum (80%) at 30 s, the earliest measurable time point, and plateauing between 10 and 30 min. Dose-response analysis revealed that maximal reduction of IL-1 binding was reached at FMLP concentrations that were also optimal for chemotaxis (50% effective dose = 5 x 10(-9) M). The loss of IL-1 binding capacity caused by FMLP was determined by a reduction in receptor number with no change in their affinity. The effect of FMLP on IL-1 receptor (IL-1R) was selective in that the PMN surface structures IL-8R, CD16, CD18, and major histocompatibility complex class I antigens were unaffected under these conditions. Loss of surface IL-1R was not due to an augumented rate of internalization. FMLP caused rapid release of a 45-kD IL-1-binding molecule identified as the IL-1 decoy RII. After FMLP-induced release, PMN reexpressed newly synthesized receptors, reaching basal levels by 4 h. FMLP-induced release of the IL-1 decoy RII did not impair the responsiveness of PMN to IL-1 in terms of promotion of survival and cytokine production. FMLP-induced release of the IL-1 decoy RII was unaffected by protein synthesis inhibitors, was blocked by certain protease inhibitors, and was mimicked by agents (the Ca++ ionophore A23187 and phorbol myristate acetate) that recapitulate elements in the signal transduction pathway of chemoattractant receptors. The time frame and concentration range of chemoattractant-induced rapid release of the IL-1 decoy RII are consistent with the view that IL-1 decoy RII release is an early event in the multistep process of leukocyte recruitment.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Chemoattractants induce rapid release of the interleukin 1 type II decoy receptor in human polymorphonuclear cells. 776 5


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>