interleukin-8 has been researched along with Uveitis* in 19 studies
1 review(s) available for interleukin-8 and Uveitis
1 trial(s) available for interleukin-8 and Uveitis
18 other study(ies) available for interleukin-8 and Uveitis
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Lithospermum erythrorhizon Siebold & Zucc. extract reduces the severity of endotoxin-induced uveitis.
Uveitis is an inflammatory eye condition that threatens vision, and effective anti-inflammatory treatments with minimal side effects are necessary to treat uveitis.. This study aimed to investigate the effects of Lithospermum erythrorhizon Siebold & Zucc. against endotoxin-induced uveitis in rat and mouse models.. Endotoxin-induced uveitis models of rats and mice were used to evaluate the effects of l. erythrorhizon treatment. Clinical inflammation scores and retinal thickness were assessed in the extract of l. erythrorhizon-treated rats. Histopathological examination revealed inflammatory cell infiltration into the ciliary body. Protein concentration, cellular infiltration, and prostaglandin-E2 levels were measured in the aqueous humor of the extract of l. erythrorhizon-treated rats. Protective effects of l. erythrorhizon on the anterior segment of the eye were examined in mice with endotoxin-induced uveitis. Additionally, we investigated the effect of l. erythrorhizon on the expression of pro-inflammatory cytokines [tumor necrosis factor alpha, interleukin-6, and interleukin-8] in lipopolysaccharide-stimulated THP1 human macrophages and examined the involvement of nuclear factor kappaB/activator protein 1 and interferon regulatory factor signaling pathways. Furthermore, three components of l. erythrorhizon were identified and assessed for their inhibitory effects on LPS-induced inflammation in RAW264.7 macrophage cells.. Treatment of the extract of l. erythrorhizon significantly reduced clinical inflammation scores and retinal thickening in rats with endotoxin-induced uveitis. Histopathological examination revealed decreased inflammatory cell infiltration into the ciliary body. The extract of l. erythrorhizon effectively reduced the protein concentration, cellular infiltration, and PG-E2 levels in the aqueous humor of rats with endotoxin-induced uveitis. In mice with endotoxin-induced uveitis, the extract of l. erythrorhizon demonstrated a protective effect on the anterior segment of the eye by reducing inflammation and retinal thickening. The extract of l. erythrorhizon suppressed the expression of pro-inflammatory cytokines (tumor necrosis factor alpha, interleukin-6, and interleukin-8) in lipopolysaccharide-induced inflammation in THP1 human macrophages, by modulating nuclear factor kappaB/activator protein 1 and interferon regulatory factor signaling pathways. Moreover, shikonin, acetylshikonin, and β, β-dimethylacryloylshikonin showed dose-dependent inhibition of nitric oxide, tumor necrosis factor alpha and interleukin-6 production in RAW264.7 macrophage cells.. The extract of l. erythrorhizon is a potential therapeutic agent for uveitis management. Administration of the extract of l. erythrorhizon led to reduced inflammation, retinal thickening, and inflammatory cell infiltration in rat and mouse models of uveitis. The compounds (shikonin, acetylshikonin, and β, β-dimethylacryloylshikonin) identified in this study played crucial roles in mediating the anti-inflammatory effects of l. erythrorhizon. These findings indicate that the extract of l. erythrorhizon and its constituent compounds are promising candidates for further research and development of novel treatment modalities for uveitis. Topics: Animals; Anti-Inflammatory Agents; Cytokines; Endotoxins; Humans; Inflammation; Interferon Regulatory Factors; Interleukin-6; Interleukin-8; Lipopolysaccharides; Lithospermum; Mice; NF-kappa B; Rats; Transcription Factor AP-1; Tumor Necrosis Factor-alpha; Uveitis | 2023 |
IL-8 Triggers Neutrophil Extracellular Trap Formation Through an Nicotinamide Adenine Dinucleotide Phosphate Oxidase- and Mitogen-Activated Protein Kinase Pathway-Dependent Mechanism in Uveitis.
To explore the mechanism underlying IL-8-induced neutrophil extracellular trap (NET) formation in patients with ocular-active Behçet's disease (BD) and the effect of inhibiting NET formation on the severity of inflammation in experimental autoimmune uveitis (EAU) mice.. The serum extracellular DNA and neutrophil elastase (NE) and IL-8 levels in patients with ocular-active BD, the expression of myeloperoxidase, NE, and histone H3Cit in IL-8-induced neutrophils isolated from healthy controls, and the effects of NETs on HMC3 cells were detected. Female C57BL/6J mice were immunized with IRBP651-670 to induce EAU and EAU mice received intravitreal injection of the CXCR2 (IL-8 receptor) antagonist SB225002 or PBS. The serum levels of extracellular DNA, NE, and keratinocyte-derived chemokine (the mouse ortholog of human IL-8) and expression of myeloperoxidase, NE, and histone H3Cit in mouse retinas were detected. Disease severity was evaluated by clinical and histopathological scores.. Serum keratinocyte-derived chemokine expression levels in EAU mice and IL-8 expression levels in patients with ocular-active BD increased. IL-8 notably increased NET formation in a dose-dependent manner through an nicotinamide adenine dinucleotide phosphate oxidase and mitogen-activated protein kinase pathway dependent mechanism. IL-8-induced NET formation damaged HMC3 cells in vitro. Pretreatment with SB225002 notably ameliorated the production of NETs in EAU mice.. Our data confirm that NET formation is induced by IL-8. IL-8-induced NET formation was found to be related to mitogen-activated protein kinase and nicotinamide adenine dinucleotide phosphate pathways. Pretreatment with the CXCR2 antagonist SB225002 alleviated neutrophil infiltration and suppressed NET formation in EAU mice. Topics: Animals; Behcet Syndrome; DNA; Extracellular Traps; Female; Histones; Humans; Interleukin-8; Mice; Mice, Inbred C57BL; Mitogen-Activated Protein Kinases; NADP; Neutrophils; Peroxidase; Uveitis | 2023 |
Could different aqueous humor and plasma cytokine profiles help differentiate between ocular sarcoidosis and ocular tuberculosis?
A cross-sectional single-center study was conducted to assess cytokine levels in aqueous humor (AH) and plasma of three different uveitis entities: definite ocular sarcoidosis (OS), definite OS associated with QuantiFERON®-TB Gold test positivity (Q + OS) and presumed tubercular uveitis (TBU).. Thirty-two patients (15 OS, 5 Q + OS, 12 TBU) were included.. Quantification of selected cytokines was performed on blood and AH samples collected before starting any treatment. Statistical analysis was conducted using the Kruskal-Wallis test, the Mann-Whitney or Fisher test and the Principal Component Analysis (PCA).. IL-6, IL-8 and IP-10 levels were higher in AH samples than in peripheral blood. In AH samples, BLC, IL-8 and IP-10 were significantly higher in definite OS than in presumptive TBU. There were no statistically significant differences in terms of cytokine levels between Q + OS and presumptive TBU. PCA showed a similar cytokine pattern in the latter two groups (IFNγ, IL-15, IL-2, IP-10, MIG), while the prevalent expression of BLC, IL-10 and MIP-3 α was seen in definite OS.. The different AH and plasma cytokine profiles observed in OS compared to Q + OS and TBU may help to differentiate OS from TBU in overlapping clinical phenotypes of granulomatous uveitis (Q + OS). Topics: Aqueous Humor; Chemokine CXCL10; Cross-Sectional Studies; Cytokines; Humans; Interleukin-8; Sarcoidosis; Tuberculosis, Ocular; Uveitis | 2022 |
Pre-Activated Granulocytes from an Autoimmune Uveitis Model Show Divergent Pathway Activation Profiles upon IL8 Stimulation In Vitro.
In the pathophysiology of autoimmune-mediated uveitis, granulocytes have emerged as possible disease mediators and were shown to be pre-activated in equine recurrent uveitis (ERU), a spontaneous disease model. We therefore used granulocytes from ERU horses to identify early molecular mechanisms involved in this dysregulated innate immune response. Primary granulocytes from healthy and ERU horses were stimulated with IL8, and cellular response was analyzed with differential proteomics, which revealed significant differences in protein abundance of 170 proteins in ERU. Subsequent ingenuity pathway analysis identified three activated canonical pathways "PKA signaling", "PTEN signaling" and "leukocyte extravasation". Clustered to the leukocyte extravasation pathway, we found the membrane-type GPI-anchored protease MMP25, which was increased in IL8 stimulated ERU granulocytes. These findings point to MMP25 as a possible regulator of granulocyte extravasation in uveitis and a role of this molecule in the impaired integrity of the blood-retina-barrier. In conclusion, our analyses show a clearly divergent reaction profile of pre-activated granulocytes upon IL8 stimulation and provide basic information for further in-depth studies on early granulocyte activation in non-infectious ocular diseases. This may be of interest for the development of new approaches in uveitis diagnostics and therapy. Raw data are available via ProteomeXchange with identifier PXD013648. Topics: Animals; Autoimmune Diseases; Granulocytes; Horse Diseases; Horses; Interleukin-8; Proteomics; Recurrence; Uveitis | 2022 |
S100 proteins, cytokines, and chemokines as tear biomarkers in children with juvenile idiopathic arthritis-associated uveitis.
Biomarkers for juvenile idiopathic arthritis-associated uveitis (JIA-U) are needed. We aimed to measure inflammatory biomarkers in tears as a non-invasive method to identify biomarkers of uveitis activity.. Tears were collected from children with JIA-U (n=20) and pediatric controls (n=20) using Schirmer strips. S100A8, A9, A12, IL-18, IL-8, IP-10, MCP-1, RANTES, and sICAM-1 were measured by ELISA and Luminex assays. Levels of biomarkers were compared between children with JIA-U and controls, and active and inactive JIA-U.. IL-8, sICAM-1, and S100A12 levels were similar between JIA-U and controls, but differed by activity. Active JIA-U had significantly increased S100A12 compared to inactive JIA-U (mean 27,722.5 pg/ML (SE 1.3) vs. 5,937.2 (1.3), p=0.002), IL-8 (73.5 [1.2] vs. 36.2 [1.2], p=0.009), and sICAM-1 (15,822.7 [1.2) vs. 8,778.0 [1.6], p=0.024).. We detected inflammatory biomarkers non-invasively in tears of children with JIA-U. IL-8, sICAM-1, and S100A12 are potential biomarkers for uveitis activity. Topics: Adolescent; Arthritis, Juvenile; Biomarkers; Child; Cross-Sectional Studies; Enzyme-Linked Immunosorbent Assay; Eye Proteins; Female; Humans; Intercellular Adhesion Molecule-1; Interleukin-8; Male; S100A12 Protein; Tears; Uveitis | 2021 |
Aqueous humor IL-8, IL-10, and VEGF levels in Fuchs' uveitis syndrome and Behçet's uveitis.
This study investigated the levels of interleukin (IL)-8, IL-10, and vascular endothelial growth factor (VEGF) in the aqueous humor (AqH) of patients with Behçet's uveitis (BU) and Fuchs' uveitis syndrome (FUS) during an inactive period and compared these levels with those in the AqH of noninflammatory healthy control subjects.. This prospective and case-control study included 33 patients (16 patients with BU and 17 patients with FUS) and 35 control subjects. IL-8, IL-10, and VEGF levels in the AqH were quantified by performing sandwich enzyme-linked immunosorbent assay. Kruskal-Wallis test was used to compare the cytokine levels in the different groups, and statistical significance was set at p < 0.05.. IL-8 levels were significantly higher in the AqH of patients with BU and FUS than in the AqH of control subjects (p < 0.001 and p < 0.001, respectively). IL-10 levels were significantly lower in the AqH of patients with BU than in the AqH of patients with FUS and of control subjects (p = 0.001 and p < 0.001, respectively). Although VEGF levels were higher in the AqH of patients with FUS than in the AqH of patients with BU and of control subjects, the difference was significant only between patients with FUS and control subjects (p < 0.001).. We observed a significant decrease in IL-10 levels in the AqH of patients with BU and a significant increase in VEGF levels in the AqH of patients with FUS compared to controls. IL-8 and VEGF levels showed no significant difference among uveitis patients. Topics: Adult; Aqueous Humor; Behcet Syndrome; Biomarkers; Case-Control Studies; Enzyme-Linked Immunosorbent Assay; Female; Humans; Interleukin-10; Interleukin-8; Male; Middle Aged; Prospective Studies; Syndrome; Uveitis; Vascular Endothelial Growth Factor A | 2019 |
Effect of SOCS1 overexpression on RPE cell activation by proinflammatory cytokines.
The purpose of this study was to investigate the in vitro effect of Suppressor Of Cytokine Signaling 1 (SOCS1) overexpression in retinal pigment epithelium (RPE) cells on their activation by pro-inflammatory cytokines IFNγ, TNFα and IL-17. Retinal pigment epithelium cells (ARPE-19) were stably transfected with the control plasmid pIRES2-AcGFP1 or the plasmid pSOCS1-IRES2-AcGFP1. They were stimulated by IFNγ (150ng/ml), TNFα (30ng/ml) or IL-17 (100ng/ml). The levels of SOCS1 mRNA were measured by real-time PCR. Signal Transducer and Activator of Transcription 1 (STAT1) phosphorylation and IκBα expression were analysed by western Blot (WB). IL-8 secretion was analysed by ELISA and expression of MHCII molecules and ICAM-1/CD54 by flow cytometry. Our data show that SOCS1 mRNA overexpression in RPE cells prevents IFNγ-induced SOCS1 mRNA increase and IFNγ-mediated STAT1 phosphorylation. Moreover, SOCS1 overexpression in RPE cells inhibits IFNγ-induced decrease of IL-8 secretion and prevents IFNγ-induced MHC II and ICAM1/CD54 upregulation. However, SOCS1 overexpression does not affect TNFα-induced IκBα degradation nor block TNFα-induced or IL-17-induced IL-8 secretion. On the contrary, IL-17-induced secretion is increased by SOCS1 overexpression. In conclusion, SOCS1 overexpression in RPE cells inhibits some IFNγ-mediated responses that lead to uveitis development. This notion raises the possibility that SOCS1 overexpression could be a novel target for treating non-infectious uveitis. However, some proinflammatory effects of TNFα and IL-17 stimulation on RPE are not blocked by SOCS1 overexpression. Topics: Cells, Cultured; Cytokines; Histocompatibility Antigens Class II; Humans; Intercellular Adhesion Molecule-1; Interferon-gamma; Interleukin-17; Interleukin-8; NF-KappaB Inhibitor alpha; Phosphorylation; Retinal Pigment Epithelium; RNA, Messenger; STAT1 Transcription Factor; Suppressor of Cytokine Signaling 1 Protein; Tumor Necrosis Factor-alpha; Uveitis | 2016 |
Ex vivo and in vitro production of pro-inflammatory cytokines in Blau syndrome.
The objective was to study both ex vivo and in vitro secretion of pro-inflammatory cytokines in patients affected by Blau syndrome (BS) and carrying p.E383K mutation in the CARD15/NOD2 gene associated with the disease. For ex vivo studies, peripheral blood mononuclear cells (PBMCs), serum from three patients and healthy controls have been collected. PBMCs have been cultured in the presence or absence of inflammatory enhancers, such as lipopolysaccharide (LPS) and muramyl dipeptide (MDP). The levels of interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor (TNF)-α and interferon (IFN)-γ were assayed by either immunoassay or array-based system. For in vitro studies, different constructs were created cloning human wild-type and p.E383K-mutated NOD2 cDNA into the expression vector pCMV-Tag2c. HEK293 cell lines were stably transfected, cultured with or without MDP and IL-8 level was assayed in their surnatants. Statistical analysis in both studies was performed using non-parametric tests. Both ex vivo and in vitro studies have not identified a significant increase in secretion of the analyzed proinflammatory cytokines. p.E383K-mutated NOD2 transfected cells express low level of IL-8. The ex vivo basal level results from both serum and PBMCs surnatants present similar levels of IL-1β, IL-6, TNF-α and IFN-γ in patients and controls. The presence of the stimulant agents (LPS and MDP), either individual or paired, does not lead to significant increases in all cytokines concentrations in patients compared to controls. Taken together, the ex vivo and in vitro data suggest that there is not a primary mediation of IL-1β and other pro-inflammatory cytokines in BS patients carrying p.E383K. Topics: Adult; Arthritis; Biomarkers; Case-Control Studies; Cytokines; Extremities; Fathers; Female; Humans; In Vitro Techniques; Interferon-gamma; Interleukin-1beta; Interleukin-6; Interleukin-8; Male; Middle Aged; Mutation; Nod2 Signaling Adaptor Protein; Nuclear Family; Pedigree; Sarcoidosis; Synovitis; Tumor Necrosis Factor-alpha; Uveitis | 2015 |
Inhibition of RPE cell sterile inflammatory responses and endotoxin-induced uveitis by a cell-impermeable HSP90 inhibitor.
Dying cells release pro-inflammatory molecules, functioning as cytokines to trigger cell/tissue inflammation that is relevant to disease pathology. Heat-shock protein 90 (HSP90) is believed to act as a danger signal for tissue damage once released extracellularly. Potential roles of HSP90 were explored in retinal pigment epithelial (RPE) inflammatory responses to necrosis. Cellular extracts can trigger ARPE-19 cell inflammatory responses, producing cytokines that lead to an increase in ARPE-19 cell monolayer permeability. Addition of recombinant HSP90β mimics the induction of chemokines IL-8 and MCP-1 in cultured RPE cells, suggesting that released HSP90 can incite RPE cell sterile inflammatory responses. Consistent with this, classical HSP90 inhibitors were shown to substantially reduce necrosis-induced cytokine production and permeability increases in ARPE-19 cells. Moreover, a cell-impermeable inhibitor, 17-N,N-dimethylaminoethylamino-17-demethoxy-geldanamycin-N-oxide, also efficiently inhibited necrosis-induced cytokine production and TNF-α/IL-1β-induced increase in ARPE-19 cell permeability in vitro and endotoxin-induced development of uveitis in vivo, suggesting that HSP90 can contribute to necrosis-induced RPE inflammatory responses. Collectively, our data identify HSP90 as a pro-inflammatory molecule in RPE cell sterile inflammatory responses. Topics: Animals; Anti-Inflammatory Agents; Benzoquinones; Cell Line; Chemokine CCL2; Disease Models, Animal; Dose-Response Relationship, Drug; Extracellular Signal-Regulated MAP Kinases; Heterocyclic Compounds, 2-Ring; HSP90 Heat-Shock Proteins; Humans; Inflammation Mediators; Interleukin-1beta; Interleukin-8; JNK Mitogen-Activated Protein Kinases; Lactams, Macrocyclic; Lipopolysaccharides; Male; Necrosis; Permeability; Protein Kinase Inhibitors; Pyrazoles; Rats; Rats, Inbred Lew; Retinal Pigment Epithelium; Signal Transduction; Time Factors; Tumor Necrosis Factor-alpha; Uveitis | 2011 |
[Concentration assessment of interleukin 8 in serum at children with uveitis].
Uveitis in children is a visual threatening disease with a complication rate of more than 75%. At the children the uveitis differs in several aspect from adults like: clinical presentation or complication of disease. The etiology of uveitis is still unknown, but T lymphocytes are generally key mediators of the pathogenesis of uveitis. In our study we evaluate IL-8 concentration in serum in uveitis patients.. Serum sample were collected from 28 uveitis patients and 20 people from control group. The level IL-8 was measured with specific enzyme- linked immunoassays ELISA methods (R & D Systems).. Level of IL-8 in uveitis group was a significant higher (p<0.04) compared with control group.. Increased levels of interleukin 8 in serum of children with uveitis may suggest innate immune mechanisms in the acute disease. Topics: Adolescent; Biomarkers; Case-Control Studies; Child; Child Welfare; Enzyme-Linked Immunosorbent Assay; Female; Humans; Interleukin-8; Male; Uveitis | 2010 |
[Effect of corticotherapy on interleukin-8 and -12 and nitric oxide production during Behçet and idiopathic uveitis].
To investigate the effect of corticotherapy on IL-8, IL-12, and nitric oxide (NO) production during idiopathic and Behçet active uveitis.. Peripheral venous blood was drawn from 70 patients with active uveitis before and during corticotherapy (32 with Behçet uveitis and 38 with idiopathic uveitis) and from 30 controls. Plasma was collected and peripheral blood mononuclear cells were separated immediately and cultured with or without Concanavaline A. IL-8 and IL-12 levels in plasma and culture supernatants were measured by specific enzyme-linked immunosorbent assay (ELISA). Nitric oxide levels were evaluated using a modified Griess method.. Before therapy, the two groups of patients showed highly significant elevation of IL-8, IL-12, and NO levels compared to control subjects. During therapy, IL-8 and nitric oxide levels were significantly lower in active idiopathic and Behçet active uveitis both in vivo and in vitro. This effect was correlated with therapy duration. In contrast, while significant reduction of IL-12 levels was observed both in vivo and in vitro in idiopathic active uveitis during therapy, this effect was observed in vitro in Behçet active uveitis but not in vivo.. Our results suggest that IL-8, IL-12, and NO are involved in the physiopathological mechanisms of idiopathic and Behçet uveitis. These three molecules showed different degrees of sensitivity to the inhibitory effect of corticoids, reflecting their different regulation by corticotherapy during active phases of the two diseases. According to our study, IL-8 can serve as a marker of inflammatory responses, while IL-12 should be used as a marker of the specific immune responses during active uveitis. Topics: Adolescent; Adrenal Cortex Hormones; Adult; Behcet Syndrome; Female; Humans; Interleukin-12; Interleukin-8; Male; Middle Aged; Nitric Oxide; Uveitis | 2008 |
Prednisolone mediated suppression of HIV-1 viral load strongly correlates with C-C chemokine CCL2: In vivo and in vitro findings.
CCL2 (MCP-1) is a proinflammatory chemokine induced in HIV-1 infection. We have previously demonstrated a significant correlation of CCL2 gene expression with HIV-1 viremia. In this study we investigated the effect of prednisolone on CCL2 gene expression and viral load in an HIV-1-infected patient receiving high-dose prednisolone for severe uveitis. We observed a >1 log reduction of HIV-1 viral load, associated with more than hundred fold reduction of CCL2 expression at day 3 of prednisolone treatment. In vitro HIV-1 infection of PBMC demonstrated reduced HIV-1 replication in the presence of prednisolone. Flow cytometric analysis revealed 50% reduction of LTR driven GFP activity by prednisolone in GHOST cells. These findings indicate that prednisolone suppresses both HIV-1 viral load and CCL2 mRNA expression, an association which might be exploited for future anti-inflammatory therapeutic strategies in HIV-1 infection. Topics: Alkynes; Anti-HIV Agents; Anti-Inflammatory Agents; Benzoxazines; Chemokine CCL2; Cyclopropanes; Drug Resistance, Viral; Flow Cytometry; Gene Expression; HIV Infections; HIV-1; Humans; In Vitro Techniques; Interleukin-8; Lamivudine; Male; Prednisolone; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Tumor Necrosis Factor-alpha; Uveitis; Viral Load; Viremia; Zidovudine | 2007 |
Hyperglycemia in streptozotocin-induced diabetes leads to persistent inflammation and tissue damage following uveitis due to reduced levels of ciliary body heme oxygenase-1.
This study investigated the heme oxygenase-1 (HO-1) and the endotoxin-induced uveitis (EIU) in diabetic streptozotocin (STZ)-hyperglycemic rats. STZ-hyperglycemic rats had impaired levels of the enzyme HO-1 within the ciliary bodies if compared with the nondiabetic rats. STZ-hyperglycemic rats also predisposed the eye to produce high levels of both the cytokines IL-1beta and CXCL8. Subsequent EIU further and significantly (P < .01) increased the cytokines production, an effect partly prevented by hemin treatment. Most importantly, hemin, an inducer of heme oxygenase expression and activity, recovered the huge number of infiltrated polymorphonuclear leukocytes PMN within the ciliary bodies associated with STZ-hyperglycemic state and EIU damage. Impairment of the stress-sensitive enzyme HO-1 in STZ-hyperglycemic rats increases and prolongs the inflammatory response to EIU. Topics: Animals; Ciliary Body; Diabetes Mellitus, Experimental; Enzyme-Linked Immunosorbent Assay; Heme Oxygenase-1; Hemin; Hyperglycemia; Inflammation; Interleukin-1beta; Interleukin-8; Lipopolysaccharides; Male; Neutrophils; Random Allocation; Rats; Rats, Sprague-Dawley; Streptozocin; Uveitis | 2006 |
The demonstration of serum interleukin 6-8, tumor necrosis factor-alpha, complement, and immunoglobulin levels in Behçet's disease with ocular involvement.
To investigate whether there are alterations in the humoral immune system in patients with Behçet's disease (BD) with ocular involvement.. Twenty-four BD patients with active uveitis and without any other manifestations of the disease were included in Group I-a. The same patients were reassessed during the convalescence period and assigned to Group I-c. Moreover, 24 age- and sex-matched healthy controls (Group II) were included in the study. Serum levels of immunoglobulin (Ig) A, IgM, complement (C) 3, C4, interleukin (IL)-6, IL-8, and tumor necrosis factor-alpha (TNF-alpha) in Groups I-a, I-c, and II were measured and compared.. IgA, C3, C4, IL-6, IL-8, and TNF-alpha levels were higher in Group I-a than in Groups I-c and II.. IgA-, C3-, C4-, IL6-, IL8-, and TNF-alpha-mediated mechanisms might be responsible for ocular lesions in BD. Topics: Adult; Antibody Formation; Behcet Syndrome; Complement System Proteins; Enzyme-Linked Immunosorbent Assay; Female; Humans; Immunoglobulins; Interleukin-6; Interleukin-8; Male; Tumor Necrosis Factor-alpha; Uveitis | 2004 |
CXC chemokine GRO is essential for neutrophil infiltration in LPS-induced uveitis in rabbits.
The purpose of this study was to investigate the role and regulation of the CXC chemokine GRO and the interaction between GRO and IL-8 in LPS-induced uveitis in rabbits. Uveitis was induced by intravitreal injection of 100 ng of LPS in rabbits. After the LPS injection, GRO was produced in aqueous humor and peaked at 24 hr. Immunohistochemistry showed that ciliary epithelial cells were responsible for production of GRO. Blocking the activity of GRO by anti-GRO serum reduced LPS-induced aqueous neutrophil counts by 80%, but did not reduce the mononuclear cell counts or protein levels or IL-8 levels. Regulation of GRO production by TNFalpha, IL-1 and IL-8 was studied. Anti-TNFalphamAb alone did not inhibit the 24 hr LPS induced GRO levels, whereas rrIL-1Ra inhibited the GRO production by 58%. The combination of anti-TNFalpha mAb and rrIL-1Ra inhibited 93% of GRO production. Although treatment with anti-IL-8 IgG inhibited the neutrophil infiltration by 66%, treatment with this antibody did not inhibit GRO production. Taken together, our results suggest that GRO is an essential mediator for neutrophil infiltration in LPS-induced uveitis in rabbits. Most of GRO production is mediated by TNFalpha and IL-1. GRO and IL-8 act in concert to mediate neutrophil infiltration. Topics: Animals; Chemokines, CXC; Immunohistochemistry; Interleukin-1; Interleukin-8; Lipopolysaccharides; Neutrophils; Rabbits; Tumor Necrosis Factor-alpha; Uveitis | 2000 |
Role and regulation of IL-8 and MCP-1 in LPS-induced uveitis in rabbits.
Intravitreal injection of lipopolysaccharide (LPS) induces leukocyte infiltration and protein leakage into the aqueous humor. In the present study, we investigated the role of IL-8 and MCP-1 and regulation of these chemokines by TNFalpha and IL-1 in LPS-induced uveitis in rabbits. After intravitreal injection of LPS, generation of IL-8 in the aqueous humor showed a biphasic pattern with the first peak at 12 hr and the second one at 24 hr, while MCP-1 was produced in a monophasic pattern and peaked at 24 hr. Immunohistochemistry showed that ciliary epithelial cells and infiltrating leukocytes were the producing cells of IL-8 and MCP-1. Administration of anti-IL-8 IgG suppressed by 66% the peak levels of LPS-induced aqueous neutrophil counts at 24 hr but did not suppress aqueous mononuclear cell counts or protein levels. anti-MCP-1 IgG inhibited aqueous mononuclear cell counts by 41% and protein levels by 28%, but did not inhibit aqueous neutrophil counts. The levels of LPS-induced aqueous IL-8 and MCP-1 at 12 hr were inhibited by anti-TNFalpha mAb but not by an IL-1 receptor antagonist (IL-1Ra), while concentrations of the two chemokines at 24 hr were inhibited by both anti-TNFalpha mAb and IL-1Ra. A combination of anti-TNFalpha mAb and rrIL-1Ra had an additive effect on the 24 hr-chemokine levels and inhibited up to 90% chemokine production. Taken together, our results show that IL-8 mediates neutrophil infiltration, while MCP-1 mediates mononuclear cell infiltration and protein leakage in LPS-induced uveitis in rabbits. Levels of aqueous IL-8 and MCP-1 at 12 hr are regulated by TNFalpha, while levels at 24 hr are regulated by TNFalpha and IL-1. Topics: Animals; Antibodies, Monoclonal; Aqueous Humor; Chemokine CCL2; Chemokines; Enzyme-Linked Immunosorbent Assay; Female; Immunoglobulin G; Immunohistochemistry; Interleukin-1; Interleukin-8; Leukocytes; Lipopolysaccharides; Rabbits; Recombinant Proteins; Statistics, Nonparametric; Tumor Necrosis Factor-alpha; Uveitis | 1999 |
The effects of betamethasone derivatives on endotoxin-induced uveitis in rats.
The anti-inflammatory effects of betamethasone and its derivatives (betamethasone 21-phosphate, betamethasone 21-acetate, betamethasone 17-valerate, clobetasol 17-propionate and betamethasone dipropionate) on endotoxin-induced uveitis (EIU) in rats was investigated. Among the compounds examined, betamethasone, betamethasone 21-phosphate, betamethasone 21-acetate and clobetasol 17-propionate strongly inhibited cell infiltration into the aqueous humor in the EIU by instillation into the eye in a dose-dependent manner (0.01-1.0%) and by systemic administration (1 mg kg-1). On the other hand, betamethasone 17-valerate and betamethasone dipropionate showed only weak inhibitory effects or enhancement of cell infiltration by instillation into the eye (0.01-1.0%) and by systemic administration (1 mg kg-1). Combined systemic administration of betamethasone dipropionate and betamethasone reduced the inhibitory effect of betamethasone on cell infiltration and gene expression of IL-1 beta. In an in vitro interleukin-8 (IL-8) release assay, betamethasone showed stronger inhibition of the IL-8 release from rat peritoneal exudate cells (PEC) than betamethasone dipropionate, and simultaneous addition of betamethasone dipropionate with betamethasone reduced the inhibitory effect of the latter. These results suggest that the betamethasone derivative betamethasone dipropionate might behave as an anti-glucocorticoid in rats. Topics: Administration, Cutaneous; Administration, Topical; Animals; Anti-Inflammatory Agents; Aqueous Humor; Betamethasone; Drug Antagonism; Drug Combinations; Endotoxins; Female; Interleukin-1; Interleukin-8; Macrophages, Peritoneal; Rats; Rats, Inbred Lew; Uveitis | 1997 |
Chemoattractant and neutrophil degranulation activities related to interleukin-8 in vitreous fluid in uveitis and vitreoretinal disorders.
To investigate whether the cytokine interleukin-8 (IL-8), a strong chemoattractant and activator for neutrophils, is responsible for neutrophil infiltration and degranulation in the eye in uveitis.. IL-8 and elastase were measured with specific enzyme-linked immunoassays in vitreous fluid samples obtained from 69 patients with various uveitis entities. Vitreous fluid of nonuveitis patients and eye bank eyes served as controls. The chemotactic activity of vitreous fluid was tested with the Boyden chamber technique.. IL-8 was detected in 45% of the vitreous fluid samples from uveitis patients and in 26% of vitreous fluid samples from nonuveitis patients. Vitreous fluid samples with IL-8 levels exceeding 100 pg/ml were chemotactic for neutrophils. This chemotactic activity could be blocked by 41% to 79% with a monoclonal anti-IL-8 antibody. Elastase levels in vitreous fluid of uveitis patients with detectable IL-8 were significantly higher than those in vitreous fluid samples with no detectable IL-8.. These results indicate that IL-8 participates in the inflammatory processes in the eye by attracting and degranulating neutrophils. It is suggested that these processes contribute to the pathogenesis of tissue destruction in uveitis. Topics: Cell Degranulation; Cells, Cultured; Chemotaxis, Leukocyte; Enzyme-Linked Immunosorbent Assay; Eye Diseases; Humans; Interleukin-8; Neutrophils; Pancreatic Elastase; Retinal Diseases; Uveitis; Vitreous Body | 1993 |