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)

We investigated the time-course release of IL-1beta and IL-8 protein as well as the steady state mRNA level of their genes in human whole blood after stimulation with LPS, beta-1,3-D-glucan and mould extracts. We compared the response of 10 non-atopic and 10 atopic individuals. In parallel, cytokine protein release and the corresponding steady state mRNA level was determined by the standard ELISA and real-time on-line RT-PCR methods, respectively. Glucan induced the highest level of IL-1beta mRNA and protein release after 3 h. IL-8 was induced at 3 h after glucan, but not after LPS, induction, which indicates different induction pathways. At the time-points found to elicit the optimal cytokine response significantly higher basal cytokine mRNA levels and significantly lower LPS induced cytokine mRNA levels were observed in the non-atopic group. Generally, mould components induced cytokine mRNA steady state to lower levels in the atopics compared to the non-atopics. In contrast, no differences were found between the two groups in their capacity to induce cytokine protein release. These findings persisted after correction for the percentage of mononuclear cells. The data supported our hypothesis that "exhaustion" of the atopic immune system elicits lower basal cytokine mRNA levels and that analysis of cytokine gene expression has the potential to differentiate between non-atopic and atopic individuals.
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PMID:Ex vivo induction of cytokines by mould components in whole blood of atopic and non-atopic volunteers. 1469 63

Glucans are fungal cell wall glucose polymers that are released into the blood of infected patients. The role of glucans in infection is unknown. We examined serum glucan and cytokine levels in intensive care unit (ICU) patients with infections. There was an inverse correlation (p<0.001) between serum glucan levels and interleukin (IL)-2), IL-4, tumor necrosis factoralpha (TNFalpha) and granulocyte macrophage-colony stimulating factor (GM-CSF) levels in infected ICU patients. The correlation between serum cytokines and serum glucan was only observed at glucan concentrations <40 pg/ml. No change was observed at serum glucan levels of >40 pg/ml. There was no correlation between serum glucan levels and systemic levels of IL-1beta, IL-5, IL-6, IL-8, IL-10 or IFNgamma. Interestingly, blood borne glucans did not suppress systemic cytokine levels in infected ICU patients, instead they were maintained at control levels. We conclude that circulating glucans may prevent cytokine upregulation in response to infection. This may represent an adaptive response to septic injury.
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PMID:At low serum glucan concentrations there is an inverse correlation between serum glucan and serum cytokine levels in ICU patients with infections. 1522 86

We have recently demonstrated that the cell wall beta-glucan of Candida albicans could be solubilized by sodium hypochlorite, followed by dimethylsulfoxide-extraction (NaClO-DMSO method). In this study, applying this method to Aspergillus spp., we prepared mycelial cell wall beta-glucan and examined its physical properties and immunotoxicological activity. The acetone-dried mycelia of Aspergillus spp. were oxidized by the NaClO-DMSO method. An analysis of (13)C NMR spectra revealed the preparations to be composed of alpha-(1 --> 3) and beta-(1 --> 3)-D-glucan. Also, the proportion of alpha-(1 --> 3) and beta-(1 --> 3)-D-glucan varied. Furthermore, a solubilized Aspergillus beta-glucan (ASBG) was prepared from OX-Asp by urea-autoclave treatment. ASBG showed limulus activity similar to Candida solubilized beta-glucan (CSBG), and there was little difference in the activity of ASBG between various Aspergillus spp. ASBG affected the production of IL-8 by human peripheral blood mononuclear cells (PBMC). ASBG should be useful for analyzing the clinical role of beta-glucan.
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PMID:The solubilization and biological activities of Aspergillus beta-(1 --> 3)-D-glucan. 1536 99

The signaling mechanism of the novel (1,4)-alpha-D-glucan (RR1) isolated from the medicinal plant Tinospora cordifolia was investigated in macrophages to evaluate its immunostimulating properties. When RAW264.7 macrophages were incubated with RR1 at 4 degrees C, the novel glucan inhibited the phagocytosis of unopsonized zymosan A bioparticles in a dose-dependent manner. RR1 also inhibited the binding and internalization of opsonized zymosan A bioparticles, although at a lower level than laminarin. Incubation of macrophages with anti-CD11b mAb followed by RR1 failed to show any inhibitory effect on RR1-induced TNF-alpha synthesis confirming that complement receptor 3 (CR3) is not involved in the opsonic binding and internalization of RR1 in macrophages unlike zymosan A. The anti-CD11b mAb has significant inhibitory effect on the zymosan A-induced tumor necrosis factor (TNF)-alpha synthesis. RR1 induced TNF-alpha synthesis in macrophages in a dose-dependent manner which can be completely inhibited by the NF-kappaB inhibitor caffeic acid phenethyl ester (CAPE) or curcumin. RR1 activated NF-kappaB in a time- and dose-dependent manner and this modulation of nuclear NF-kappaB activity is associated with the degradation of I-kappaB alpha thus facilitating the translocation of NF-kappaB into the nucleus. RR1-induced NF-kappaB activity peaks at 8 h of RR1 stimulation while I-kappaB alpha degradation occurred within 1 h of stimulation. RR1-induced NF-kappaB activation occurred through TLR6 signaling as evidenced by the synthesis of IL-8 in TLR6-transfected HEK293 cells. These results show that the novel (1,4)-alpha-D-glucan from Tinospora cordifolia activates the immune system through the activation of macrophages that occurs through TLR6 signaling, NF-kappaB translocation and cytokine production.
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PMID:Mechanism of macrophage activation by (1,4)-alpha-D-glucan isolated from Tinospora cordifolia. 1705 72

Yeast, fungal, and dietary beta-glucans have immune-modulating effects in vitro and in vivo, as thought, mainly by affecting leukocytes; however, effects of oat beta-glucan on enterocytes have never been studied. As recognized, supplying oat beta-glucans as such to cells in culture directly is difficult because of solubility problems. Therefore, six ileostomic patients consumed, in random order, a control diet or an oat beta-glucan enriched diet (5 g) and from the collected ileostomic content, fecal water was prepared and added to two small intestinal cell lines (INT407, Caco-2) and two colon cell lines (HT29, T84) together with a cytokine cocktail (IL-1beta + INFgamma + TNFalpha). Several parameters reflecting immune-modulation were measured. As compared to placebo fecal water, beta-glucan enriched fecal water significantly increased IL-8 production in HT29 (5.0%; p = 0.046) and INT407 cells (22.0%; p = 0.028). Intercellular adhesion molecule (ICAM)-1 expression increased in T84 (11.0%; p = 0.028) and Caco-2 cells (20.4%; p = 0.075). These immune-stimulating effects were confirmed by enhancement of inflammatory expression profiles, as determined with an antibody array. Our findings show immune enhancement by fecal water from ileostomic patients consuming oat beta-glucan both in small intestinal and colon cell lines after stimulation, which is in agreement with documented effects in leukocytes. Whether these immune-stimulating effects on enterocytes contribute to the enhanced protection of the host against invading pathogens as observed both in animals and in humans, as well as the underlying mechanism, needs further evaluation.
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PMID:Fecal water from ileostomic patients consuming oat beta-glucan enhances immune responses in enterocytes. 1723 May 85

Water-insoluble alpha-glucans are synthesized from sucrose by glucosyltransferase-I of mutans streptococci and play an important role in the development of dental plaque. Several types of beta-glucans in fungal cell wall components and water-soluble alpha-glucans from Streptococcus mutans are known to modulate innate immunity. In the present study, we investigated whether water-insoluble alpha-glucans also induced inflammatory innate immune responses. Our results showed that water-insoluble alpha-glucans synthesized by Streptococcus sobrinus activated mouse peritoneal exudate macrophages to produce pro-inflammatory cytokines. The immunological responses were not due to contamination by sucrose, water-soluble alpha-glucan, lipopolysaccharide, or peptidoglycan. Furthermore, human monocytes stimulated by water-insoluble alpha-glucans produced TNF-alpha and IL-8, while human polymorphonuclear cells were activated by water-insoluble alpha-glucans, resulting in chemotaxis and hydrogen peroxide production. The results demonstrated that water-soluble alpha-glucans modulate macrophage- and granulocyte-induced inflammatory immune responses, and suggest that inflammation induced by those alpha-glucans is associated with the development of periodontal diseases.
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PMID:Inflammatory immune responses by water-insoluble alpha-glucans. 1731 56

The monocyte activation test (MAT) has been introduced as an alternative for the detection of pyrogens in pharmaceuticals with the rabbit pyrogen test or the Limulus amebocyte lysate (LAL) test. The basis of the MAT is that pyrogens, via Toll-like receptors (TLRs) expressed on monocytes, stimulate cytokine production. Here, we report that, at concentrations that did not induce whole blood cytokine production when tested separately, (1-->3)-beta-D-glucans powerfully co-stimulated cytokine production (IL-6/IL-8) induced by ligands for TLR1/2, TLR2/6, TLR4, and TLR5. Experiments were performed to investigate the involvement of particular (1-->3)-beta-D-glucan receptors such as dectin-1. Spleen tyrosine kinase (Syk) inhibition attenuated the potentiating effects of (1-->3)-beta-D-glucans on TLR-induced cytokine production, suggesting that dectin-1 was involved. However, experiments with low molecular (1-->3)-beta-D-glucans such as laminarin argued against the involvement of dectin-1 in the co-stimulatory effects of (1-->3)-beta-D-glucans. Thus, although the receptors involved in the co-stimulatory actions of (1-->3)-beta-D-glucans on TLR-induced cytokine production are yet to be elucidated, it is clear that (1-->3)-beta-D-glucans may greatly affect MAT results and, when undetected in pharmaceuticals, may give rise to serious side-effects in patients co-exposed to other elicitors of innate immunity, such as during infections.
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PMID:Potentiation of Toll-like receptor-induced cytokine production by (1-->3)-beta-D-glucans: implications for the monocyte activation test. 1762 56

Candida albicans, Saccharomyces cerevisiae and their cell wall components, zymosan and glucan, have been shown to stimulate interleukin-8 (IL-8/CXCL-8) production by intestinal epithelial cell-like Caco-2 cells pre-cultured with 10 mM butyric acid. We examined in this study whether these yeasts also altered the production of other cytokines and cyclooxygenases (COXs) by Caco-2 cells. Culturing Caco-2 cells with 10 mM butyric acid and 15% FBS for 4 days enhanced the basal levels of mRNA encoding IL-6, IL-8, IL-18, monocyte chemoattractant protein (MCP)-1, stem cell factor, transforming growth factor (TGF)-beta1, TGF-beta3, tumor necrosis factor (TNF)-alpha, COX-1, and COX-2, but not of granulocyte-macrophage colony-stimulating factor (GM-CSF) and TGF-beta2. The inclusion of live S. cerevisiae or C. albicans further enhanced the production of IL-8, but not of the other cytokines and COXs. The non-pathogenic yeasts, C. kefyr, C. utilis, C. versatilis, Kluyveromyces lactis, K. marxianus, Schizosaccharomyces pombe and Zygosaccharomyces rouxii, used for the production of fermented foods and probiotics, and the opportunistic pathogens, C. glabrata, C. krusei, C. parapsilosis and C. tropicalis, isolated from human tissue samples also enhanced IL-8 secretion by Caco-2 cells.
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PMID:Cytokine responses of intestinal epithelial-like Caco-2 cells to non-pathogenic and opportunistic pathogenic yeasts in the presence of butyric acid. 1792 16

The acute effects of pure inhaled glucan on respiratory inflammation remain inconclusive and not sufficiently examined with regards to the simultaneous interaction of glucan, endotoxin (lipopolysaccharide, LPS), and house dust in airway inflammation. This study aims at determining effects of simultaneous exposure to office dust and glucan on nasal and pulmonary inflammation. This is relevant for humans with occupational exposure in waste handling and farming and buildings with mold problems. Office dust collected from Danish offices was spiked with 1% (1-3)-beta-glucan (curdlan). Guinea pig nasal cavity volume was measured by acoustic rhinometry (AR) and animals were exposed by inhalation for 4 h to curdlan-spiked dust, unspiked dust, purified air (negative controls), or LPS (positive controls). After exposure (+5 h) or the following day (+18 h), measurements were repeated by AR and followed by bronchoalveolar lavage (BAL). Total and differential cell counts, interleukin (IL)-8 in BAL fluid, and change in nasal volume were compared between groups. A 5-10% increase in nasal volume was seen for all groups including clean air except for a significant 5% decrease for spiked-dust inhalation (+18 h). No marked differences were observed in BAL cells or IL-8 except in LPS-exposed controls. The delayed decrease of nasal cavity volume after exposure to glucan spiked dust suggests a slow effect on the upper airways for curdlan and office dust together, though no pulmonary response or direct signs of inflammation were observed. Glucan-spiked office dust exposures produced a delayed nasal subacute congestion in guinea pigs compared to office dust alone, but extrapolated to nasal congestion in humans, paralleling the nasal congestion seen in human volunteers exposed to the same dust, this may not have clinical importance.
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PMID:Acute effect of glucan-spiked office dust on nasal and pulmonary inflammation in guinea pigs. 1796 63

Most invasive fungal infections such as candidemia are frequent in patients with hematologic malignancies. We measured cytokines/chemokines (IL-6, IL-8, monocytic chemoattractant protein 1, RANTES and epithelial neutrophil-activating peptide 78), soluble molecules (sFas, sE-selectin and soluble vascular cell adhesion molecule 1) and platelet activation markers (soluble CD40 ligand, sP-selectin and platelet-derived microparticles) in patients with hematologic malignancies under prophylactic treatment with an antifungal drug (fosfluconazole). We classified patients into 2 groups by the level of beta-D-glucan. The level of C-reactive protein was higher in the high beta-D-glucan group (>5 pg/ml) than in the low beta-D-glucan group. However, there were no differences in the levels of other parameters (peripheral blood cells, glutamic-oxaloacetic transaminase, glutamic-pyruvic transaminase, lactate dehydrogenase, blood urea nitrogen and creatinine). Patients in the high beta-D-glucan group exhibited a significant elevation of several chemokines, soluble molecules and platelet activation markers compared with those in the low beta-D-glucan group, but the levels of IL-8, monocytic chemoattractant protein 1 and sFas did not differ significantly. The levels of C-reactive protein and IL-6 increased significantly after 1 or 2 weeks on fosfluconazole in both groups. In contrast, the high beta-D-glucan group exhibited a significant decrease in chemokines, soluble markers and platelet-derived microparticles compared with the low beta-D-glucan group after treatment with fosfluconazole, although the patients in the low beta-D-glucan group exhibited no significant changes. Furthermore, the levels of RANTES, epithelial neutrophil-activating peptide 78, soluble vascular cell adhesion molecule 1 and sE-selectin correlated positively with platelet-derived microparticles in the high beta-D-glucan group. These findings suggest that fungal infection may modulate the vascular events in which some platelet-related chemokines are involved.
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PMID:Elevation of activated platelet-dependent chemokines and soluble cell adhesion molecules in patients with hematologic malignancies and high levels of beta-D-glucan. 1833 12


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