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

The effect of interleukin-8 (IL)-8 on human B cell growth, as determined by thymidine uptake and viable cell numbers was studied. IL-8 inhibited IL-4-induced growth of B cells costimulated with anti-mu antibodies (Ab) or Staphylococcus aureus Cowan strain I (SAC) in a dose-dependent fashion. In contrast, IL-8 did not inhibit IL-2-induced growth of B cells. The IL-8-mediated inhibition was specific, since it was blocked by anti-IL-8 mAb but not by control IgG1. Moreover, anti-tumor necrosis factor-alpha (anti-TNF-alpha) Ab blocked IL-8-mediated inhibition. On the other hand, TNF-alpha, but not other cytokines including IL-1 beta, IL-3, IL-5, IL-6, interferon-alpha (IFN-alpha) or IFN-gamma, inhibited IL-4-mediated growth, and inhibition by TNF-alpha was blocked by anti-TNF-alpha Ab but not by control IgG. IL-4 had no effect on TNF-alpha binding by B cells while it decreased TNF-alpha production by B cells. IL-8 had no effect in binding of IL-4, IL-2 or TNF-alpha by B cells, however, it enhanced TNF-alpha production by B cells. These results indicate that IL-8 inhibited IL-4-induced human B cell growth by enhancement of endogenous TNF-alpha production.
Eur J Immunol 1994 Dec
PMID:Interleukin-8 differentially modulates interleukin-4- and interleukin-2-induced human B cell growth. 780 53

This study examines the ability of HT-29 human colonic epithelial cells to stimulate neutrophil migration and adhesion. Interleukin-8 (IL-8), a potent neutrophil chemoattractant, was detected in conditioned media from both unstimulated (1.1 ng/ml) and IL-1 beta-stimulated (16.1 ng/ml) HT-29 cultures. Conditioned medium from IL-1 beta-exposed HT-29 cells stimulated neutrophil migration (395% of control, P < 0.01), and this effect was completely inhibited by anti-IL-8 antibody. HT-29 medium also induced shedding of neutrophil L-selectin and increased expression of neutrophil CD11/CD18 adhesion receptors. Coculture of HT-29 cells with human endothelial cell monolayers resulted in increased neutrophil transendothelial migration (169% of control, P < 0.01), which was blocked by both anti-IL-8 and anti-CD18 antibody. Northern hybridization analysis demonstrated increased levels of mRNA for IL-8 and intercellular adhesion molecule-1 (ICAM-1) in cytokine-treated HT-29 cells. Cytokine stimulation of HT-29 monolayers was also associated with increased neutrophil adhesion to these cells. Neutrophil-HT-29 cell adhesion was blocked by monoclonal antibodies to neutrophil CD18 or to ICAM-1 on the HT-29 cells (86% and 56% inhibition, respectively, P < 0.01 for both). These data suggest that IL-8 secretion by activated colonic epithelial cells may contribute to neutrophil extravasation and tissue infiltration in intestinal inflammation.
Am J Physiol 1994 Dec
PMID:IL-8 secretion and neutrophil activation by HT-29 colonic epithelial cells. 781 Jun 67

Major trauma and consecutively associated infectious complications have a major impact on the mechanisms of the specific immune response and the nonspecific inflammatory reaction. The trauma-induced host defense abnormalities become strikingly evident with the analysis of cytokine synthesis patterns. The dissociation of cell-mediated immune responses following trauma is based upon an overrepresentation of suppressor-active monocytes and inadequate T-cell help in parallel. Corresponding dysregulation of cytokine production appears within many facets. Complement, endotoxin and antigen antibody complexes cause a massive activation of monocytes with an abnormal release of essential mediators, like PGE2, IL-1, IL-6, IL-8, TGF-beta and TNF-alpha. The regulation of cytokine synthesis under stressful conditions is differentially regulated for the individual mediators, either on a transcriptional or a posttranscriptional level. In our opinion, the endogenous provisions of the organism for survival following major injury are inadequate and from this hypothesis we derive the necessity for a substantial exogenous therapeutic intervention. The primary target of modern immunotherapy must be to inhibit the conversion of a systemic inflammatory reaction in immunocompromised patients towards a status of bacterial sepsis. Different approaches appear to be feasible to avoid the development of late multiorgan failure. These interventions have to be utilized preventively in a controlled manner as early as possible after trauma has occurred, and they must effectively protect different cell systems (lymphocytes, monocytes, PMNs and endothelial cells).
Immun Infekt 1994 Dec
PMID:[Immune mechanisms of post-traumatic hyperinflammation and sepsis]. 782 50

Here we describe the cloning of a full-length cDNA encoding a neutrophil chemoattractant peptide, ENA-78, from human platelets. The cDNA encodes a predicted sequence of 114 amino acids and contains the Cys motif C-X-C found in other members of the alpha-chemokine family which also includes interleukin 8 (IL-8). ENA-78 has a high degree of sequence identity with other platelet-derived chemokines which also share overlapping chemotactic activities such as GRO alpha and the neurophil-activating peptide 2 (NAP-2; derived by proteolytic cleavage of the connective-tissue-activating peptide III (CTAP-III)).
Gene 1994 Dec 30
PMID:Cloning of a full-length cDNA encoding the neutrophil-activating peptide ENA-78 from human platelets. 782 1

The effects of ulinastatin on the serum interleukin 8 and 6 (IL-8, 6), granulocyte elastase (GEL), creatinphosphokinase (CK) and CK-MB were studied during open heart surgery under cardiopulmonary bypass (CPB). Eleven patients (group I) did not receive ulinastatin. Thirteen patients (group II) received 600,000 units of ulinastatin intravenously before CPB and before declamping of aorta and 12 patients (group III) received 300,000 units more added in the priming solution. The serum concentration of IL-8 and 6 increased at 60, 120, 180 min. after reperfusion compared with the preoperative value in the three groups. But, at each time point after reperfusion, IL-8 and 6 levels in group II and III were significantly lower (P < 0.01) than those in group I. GEL increased progressively after reperfusion in the three groups. There was no significant difference in the three groups with CK-MB as well CK release. These results suggest that ulinastatin is useful for protection of reperfusion injury after myocardial ischemia since ulinastatin suppresses production of IL-8 and 6.
Masui 1994 Dec
PMID:[The inhibitory effects of ulinastatin on the increase of interleukin 8 and 6 during open heart surgery]. 783 97

We examined the in vitro release of interleukin 8 (IL-8), interleukin 10 (IL-10), and interleukin 12 (IL-12) by alveolar macrophages from normal volunteers and HIV-1-infected subjects. Normal volunteers had very low levels of IL-8 and IL-10 and undetectable IL-12 in the cell-free bronchoalveolar lavage fluid (BALF). Asymptomatic HIV-1-infected subjects had elevated levels of IL-8 and IL-10 in their BALF, and HIV-1-infected subjects with nonspecific interstitial pneumonitis (NIP) or infected with Pneumocystis carinii had the highest BALF levels of IL-10 and IL-8. It was found that alveolar macrophages from asymptomatic HIV-1 subjects and from NIP subjects spontaneously released elevated IL-8, IL-10, and IL-12. However, AIDS subjects infected with P. carinii had cells that released elevated levels of IL-10 and IL-8, but low levels of IL-12. When alveolar macrophages were stimulated with Staphylococcus aureus Cowan (SAC), cells from normal volunteers responded with a considerably increased release of IL-8, IL-10, and IL-12; cells from HIV-1-infected subjects without P. carinii infection responded with a moderate increase in release of all three monokines. SAC stimulation did not enhance the release of monokines by cells from AIDS subjects with P. carinii infection, and IL-12 levels remained low. There was no strict relationship between spontaneous cytokine release and p24 HIV-1 antigen expression by alveolar macrophages. Finally, we showed that neutralizing IL-10 production by alveolar macrophages from AIDS subjects substantially increased IL-12 releasability.(ABSTRACT TRUNCATED AT 250 WORDS)
AIDS Res Hum Retroviruses 1994 Dec
PMID:Dysregulation of interleukin 8, interleukin 10, and interleukin 12 release by alveolar macrophages from HIV type 1-infected subjects. 788 21

Recently, we described the cloning and expression of a human cDNA which is the homologue to P600, a gene transcribed by mouse Th2 clones. Based on its activities on human monocytes and B cells this gene was designated IL-13. In the present study we investigated the effects of IL-13 alone or in combination with IL-4, IFN-gamma, or IL-10 on human monocytes. IL-13 induced significant changes in the phenotype of monocytes. Like IL-4, it enhanced the expression of CD11b, CD11c, CD18, CD29, CD49e (VLA-5), class II MHC, CD13, and CD23, whereas it decreased the expression of CD64, CD32, CD16, and CD14 in a dose-dependent manner. IL-13 induced up-regulation of class II MHC Ag and its down-regulatory effects on CD64, CD32, and CD16 expression were prevented by IL-10. IFN-gamma could also partially prevent the IL-13-induced down-regulation of CD64, but not that of CD32 and CD16. However, IL-13 strongly inhibited spontaneous and IL-10- or IFN-gamma-induced ADCC activity of human monocytes toward anti-D coated Rh+ erythrocytes, indicating that the cytotoxic activity of monocytes was inhibited. Furthermore, IL-13 inhibited production of IL-1 alpha, IL-1 beta, IL-6, IL-8, IL-10, IL-12 p35, IL-12 p40, macrophage inflammatory protein-1 alpha, granulocyte/macrophage-CSF, granulocyte-CSF, IFN-alpha, and TNF alpha by monocytes activated with LPS. In contrast, IL-13 enhanced the production of IL-1 ra by these cells. Similar results on cytokine production were observed or have been obtained with IL-4. Thus IL-13 shares most of its activities on human monocytes with IL-4, but no additive or synergistic effects of IL-4 and IL-13 on human monocytes were observed, suggesting that these cytokines may share common receptor components. Taken together, these results indicate that IL-13 has anti-inflammatory and important immunoregulatory activities.
J Immunol 1993 Dec 01
PMID:Effects of IL-13 on phenotype, cytokine production, and cytotoxic function of human monocytes. Comparison with IL-4 and modulation by IFN-gamma or IL-10. 790 77

The interleukin-2 (IL-2) receptor gamma is an indispensable functional component of IL-2, IL-4, and IL-7 receptors, and thus, is denoted the common gamma chain, gamma c. The present study was undertaken to determine whether human polymorphonuclear neutrophils (PMNs) expressed gamma c chain. Reverse transcription-polymerase chain reaction and Northern blot analysis showed that fresh human PMN constitutively expressed a remarkable level of gamma c mRNA, which is of the size and intensity of that from the peripheral blood mononuclear cells (PBMCs). Granulocyte macrophage-colony stimulating factor, IL-2, and IL-8, which are known to activate PMN functions, failed to regulate the gamma c gene expression. Western blot analysis with a rabbit anti-gamma c polyclonal antibody identified 64-, 58-, and 50-kD gamma c bands in lysates from PMN, but only 64- and 58-kD bands from PBMCs. After the PMNs and PBMCs were treated with tunicamycin to prevent N-linked glycosylation, Western blot analysis detected a single 39-kD band, which is equal to the calculated molecular weight from the cloned cDNA. Thus, our results indicate that PMNs constitutively express high levels of gamma c and the three forms detected are caused by different glycosylation of a protein translated from a single mRNA species.
Blood 1994 Dec 01
PMID:Expression of interleukin-2 receptor gamma chain on human neutrophils. 794 44

Analysis of synthetic tri- and tetrapeptides has previously indicated that N-formylation is required for high biological activity when they react with the phagocyte N-formylpeptide receptor, suggesting that the natural ligand for the receptor is from bacterial and/or mitochondrial sources. To explore this requirement further, we synthesized the pentapeptide methionyl-norleucyl-leucyl-phenylalanyl-phenylalanine (MNleLFF) and studied the effects of different NH2-terminal modifications on its activity. N-formyl-MNleLFF induced transient alterations of [Ca2+]i and superoxide production in human neutrophils with 10- and 100-fold greater potency, respectively, than the proto-type N-formylpeptide, N-formylmethionyl-leucyl-phenylalanine (fMLF). Surprisingly, N-acetyl-MNleLFF was a potent as N-formyl-MNleLFF. Moreover, the unacylated counterpart H-MNleLFF was also highly active, having an EC50 for calcium mobilization of 10 nM, and for respiratory burst activation of 100 nM. All three pentapeptides could completely desensitize calcium transients elicited by stimulation of neutrophils with fMLF, whereas the neutrophil chemoattractants C5a and interleukin 8 only weakly affected fMLF-induced transients, suggesting that they activate neutrophils via the same receptor as fMLF. Finally, all three pentapeptides activated the recombinant human N-formylpeptide receptor expressed in frog oocytes, but did not effectively activate related phagocyte receptors. These data broaden the potential sources of natural ligands for the N-formyl-peptide receptor from N-formylated bacterial and mitochondrial products to other nonformylated endogenous peptides.
J Exp Med 1994 Dec 01
PMID:A high potency nonformylated peptide agonist for the phagocyte N-formylpeptide chemotactic receptor. 796 94

The connective tissue-activating peptide III (CTAP-III), which is released from activated platelets, represents an inactive precursor of the chemokine neutrophil-activating peptide 2 (NAP-2). Leukocytes and leukocyte-derived proteases have been found to convert CTAP-III into NAP-2 by proteolytic cleavage at the N terminus. We demonstrate here that rapid and efficient formation of NAP-2 is mediated by neutrophil granulocytes (PMN) but not by monocytes or lymphocytes. However, as seen in a degranulation assay, neutrophils processing CTAP-III did not become activated by the generated NAP-2 and even exhibited decreased responsiveness to high doses of NAP-2 or IL-8, but not to FMLP. The desensitizing effect, being maximal already after 5 min of preincubation with CTAP-III, was not mediated through binding of the precursor to specific receptors but correlated with the rapid down-modulation of common NAP-2/IL-8 high affinity binding sites. A similar functional and receptor desensitization was observed in PMN pre-exposed to nonstimulatory doses of NAP-2. Specific inhibition of the CTAP-III-cleaving enzyme by the serine protease inhibitor aprotinin abrogated the CTAP-III, but not the NAP-2-mediated effects. Desensitization of PMN by CTAP-III was due to NAP-2 generated by proteolytic truncation of CTAP-III. Our results suggest that CTAP-III may regulate PMN activation by protecting processing cells from premature activation.
J Immunol 1994 Dec 15
PMID:Connective tissue-activating peptide III desensitizes chemokine receptors on neutrophils. Requirement for proteolytic formation of the neutrophil-activating peptide 2. 798 67


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