interleukin-8 has been researched along with Anaphylaxis* in 11 studies
2 review(s) available for interleukin-8 and Anaphylaxis
Article | Year |
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Neutrophil chemotactic factor of anaphylaxis.
Topics: Anaphylaxis; Animals; Asthma; Chemical Phenomena; Chemistry; Chemotactic Factors; Food Hypersensitivity; Guinea Pigs; Humans; Inflammation; Interleukin-8; Lung; Mast Cells; Time Factors | 1983 |
Chemotactic mediators.
Topics: Anaphylaxis; Animals; Bronchial Spasm; Chemokines, C; Chemotactic Factors; Chemotactic Factors, Eosinophil; Chemotaxis, Leukocyte; Humans; Immunoglobulin E; Inflammation; Interleukin-8; Kinetics; Lymphokines; Mast Cells; Molecular Weight; Rats; Sialoglycoproteins | 1983 |
9 other study(ies) available for interleukin-8 and Anaphylaxis
Article | Year |
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The effect of hymenoptera venom immunotherapy on neutrophils, interleukin 8 (IL-8) and interleukin 17 (IL-17).
Venom immunotherapy (VIT) is an effective treatment method and is addressed to patients with a history of an anaphylactic reaction to Hymenoptera stings. However, the immunological mechanisms of protection have not been explained yet. The objective of this study was to analyze neutrophils, interleukin 8 (IL-8) and interleukin 17 (IL-17) before and after the initial phase of the immunotherapy.. Overall, 40 individuals, including 20 wasp venom sensitized and 20 bee venom sensitized patients, were included in the study. The patients had had a history of severe allergic reactions type III and IV according to Mueller's classification. An ultra-rush VIT protocol was used in this study. The concentration of serum IL-8 and IL-17A was determined using the ELISA enzymatic method.. The authors demonstrated a significant rise in the IL-8 level after the immunotherapy, compared to baseline (14.9 vs. 24.7, p < 0.05). The rise in the neutrophils level was also noticeable but proved to be barely out of the range of statistical significance (4.3 vs. 5.0, p = 0.06). The shift in IL-17A was negligent and not statistically significant in the paired samples t-test (1.6 vs. 1.5, p = 0.34).. Venom immunotherapy induces neutrophils and IL-8 activity after 2 days. After the desensitization, the level of IL-17A did not change. Int J Occup Med Environ Health. 2020;33(6):811-7. Topics: Adult; Anaphylaxis; Animals; Arthropod Venoms; Bees; Desensitization, Immunologic; Female; Humans; Insect Bites and Stings; Interleukin-17; Interleukin-8; Leukocyte Count; Male; Middle Aged; Neutrophils; Wasps | 2020 |
Inhibition of Mast Cell-Mediated Allergic Responses by Arctii Fructus Extracts and Its Main Compound Arctigenin.
The Arctium lappa seeds (Arctii Fructus) and its major active compound, arctigenin (ARC), are known to have anticancer, antiobesity, antiosteoporosis, and anti-inflammatory activities. However, the effect of Arctii Fructus and ARC on mast cell-mediated allergic inflammation and its associated mechanism have not been elucidated. Therefore, we attempted to investigate the antiallergic activity of Arctii Fructus and ARC on mast cells and experimental mouse models. Arctii Fructus water extract (AFW) or ethanol extract (AFE) and ARC reduced the production of histamine and pro-inflammatory cytokines such as interleukin (IL)-1β, IL-6, IL-8, and TNF-α in mast cells. AFW, AFE, and ARC inhibited phosphorylation of MAPKs and NF-κB in activated mast cells. Moreover, IgE-mediated passive cutaneous anaphylaxis and compound 48/80-induced anaphylactic shock were suppressed by AFW, AFE, and ARC administration. These results suggest that Arctii Fructus and ARC are potential therapeutic agents against allergic inflammatory diseases. Topics: Anaphylaxis; Animals; Anti-Allergic Agents; Arctium; Furans; Humans; Interleukin-6; Interleukin-8; Lignans; Male; Mast Cells; Mice; Mice, Inbred ICR; Plant Extracts; Tumor Necrosis Factor-alpha | 2017 |
Apigenin inhibits the expression of IL-6, IL-8, and ICAM-1 in DEHP-stimulated human umbilical vein endothelial cells and in vivo.
Di-(2-ethylhexyl) phthalate (DEHP) in house dust is associated with asthma and allergic inflammatory symptoms in children. This study aimed to examine an inhibitory effect of a flavonoid apigenin on DEHP-stimulated inflammatory responses in human umbilical vein endothelial cells (HUVECs). We found that apigenin significantly suppressed DEHP-stimulated expression of intercellular adhesion molecule-1 (ICAM-1) at the mRNA and protein levels and subsequently inhibited the adhesion of THP-1 monocytic cells to HUVECs. Treatment with apigenin also led to a dose-dependent inhibition of mRNA and protein expression of interleukin (IL)-6 and IL-8 in DEHP-stimulated HUVECs. Moreover, pretreatment with apigenin partially inhibited the DEHP-induced activation of c-Jun N-terminal kinase (JNK) but not the degradation of IκBα or the phosphorylation of extracellular-regulated kinase (ERK)1/2, indicating that the inhibitory effect of apigenin on the expression of IL-6, IL-8, and ICAM-1 may be mediated by JNK pathway but not IκBα/nuclear factor-κB or ERK/mitogen-activated protein kinase pathway. Furthermore, apigenin reduced the release of IL-6, IL-8, and ICAM-1 and inhibited compound 48/80-induced systemic anaphylaxis in vivo. These results suggest that apigenin can be used as a therapeutic means for the treatment of DEHP-associated allergic disorders. Topics: Anaphylaxis; Animals; Apigenin; Cells, Cultured; Diethylhexyl Phthalate; Extracellular Signal-Regulated MAP Kinases; Female; Human Umbilical Vein Endothelial Cells; Humans; Hypersensitivity; I-kappa B Kinase; Inflammation; Intercellular Adhesion Molecule-1; Interleukin-6; Interleukin-8; JNK Mitogen-Activated Protein Kinases; MAP Kinase Signaling System; Mice; Mice, Inbred BALB C; p-Methoxy-N-methylphenethylamine; Phosphorylation; RNA, Messenger | 2012 |
Anti-allergic inflammatory activity of the fruit of Prunus persica: role of calcium and NF-kappaB.
Mast cell-mediated allergic symptoms are involved in many diseases, such as asthma and sinusitis. In this study, we investigated the effect of ethanol extract of fruits of Prunus persica (L) Batsch (FPP) on the mast cell-mediated allergic inflammation and studied the possible mechanism of action. FPP dose-dependently inhibited compound 48/80-induced systemic anaphylaxis and immunoglobulin E-mediated local allergic reactions. Histamine releasing from mast cells was reduced by FPP, which was mediated by modulation of intracellular calcium. In addition, FPP attenuated the phorbol 12-myristate 13-acetate and calcium ionophore A23187 (PMACI)-stimulated expression and secretion of pro-inflammatory cytokines in human mast cells. The inhibitory effect of FPP on pro-inflammatory cytokines was nuclear factor (NF)-kappaB dependent. Our findings provide evidence that FPP inhibits mast cell-derived allergic inflammation and involvement of calcium and NF-kappaB in these effects. Topics: Anaphylaxis; Animals; Anti-Allergic Agents; Anti-Inflammatory Agents; Blotting, Western; Calcium; Calcium Signaling; Cytokines; Histamine Release; Indicators and Reagents; Interleukin-8; Male; Mast Cells; Mice; Mice, Inbred ICR; NF-kappa B; p-Methoxy-N-methylphenethylamine; Passive Cutaneous Anaphylaxis; Plant Extracts; Prunus; Reverse Transcriptase Polymerase Chain Reaction; Tumor Necrosis Factor-alpha | 2010 |
RGS13 controls g protein-coupled receptor-evoked responses of human mast cells.
IgE-mediated mast cell degranulation and release of vasoactive mediators induced by allergens elicits allergic responses. Although G protein-coupled receptor (GPCR)-induced signals may amplify IgE-dependent degranulation, how GPCR signaling in mast cells is regulated remains incompletely defined. We investigated the role of regulator of G protein signaling (RGS) proteins in the modulation of these pathways in human mast cells. Several RGS proteins were expressed in mast cells including RGS13, which we previously showed inhibited IgE-mediated mast cell degranulation and anaphylaxis in mice. To characterize how RGS13 affects GPCR-mediated functions of human mast cells, we analyzed human mast cell lines (HMC-1 and LAD2) depleted of RGS13 by specific small interfering RNA or short hairpin RNA and HMC-1 cells overexpressing RGS13. Transient RGS13 knockdown in LAD2 cells lead to increased degranulation to sphingosine-1-phosphate but not to IgE-Ag or C3a. Relative to control cells, HMC-1 cells stably expressing RGS13-targeted short hairpin RNA had greater Ca(2+) mobilization in response to several natural GPCR ligands such as adenosine, C5a, sphingosine-1-phosphate, and CXCL12 than wild-type cells. Akt phosphorylation, chemotaxis, and cytokine (IL-8) secretion induced by CXCL12 were also greater in short hairpin RGS13-HMC-1 cells compared with control. RGS13 overexpression inhibited CXCL12-evoked Ca(2+) mobilization, Akt phosphorylation and chemotaxis. These results suggest that RGS13 restricts certain GPCR-mediated biological responses of human mast cells. Topics: Adenosine; Allergens; Anaphylaxis; Animals; Antigens; Calcium; Cell Degranulation; Cell Line; Chemokine CXCL12; Chemotaxis; Complement C5a; Humans; Immunoglobulin E; Interleukin-8; Ligands; Lysophospholipids; Mast Cells; Mice; Phosphorylation; Proto-Oncogene Proteins c-akt; Receptors, G-Protein-Coupled; RGS Proteins; RNA, Small Interfering; Sphingosine | 2008 |
Apoptotic cell death of neutrophils in development of skin lesions of patients with anaphylactoid purpura.
The participation of apoptotic cell death of neutrophils in the development of skin lesions of patients with anaphylactoid purpura was examined by the in situ specific labeling of fragmented DNA. In the early stage of the skin lesions, there were few positively stained nuclei in infiltrating cells. The number of positive cells increased markedly in the fully developed stage of the lesions. A number of neutrophils were stained positively. Finally, a few fragmented nuclei were still positive in the late stage of the lesions. It was therefore suggested that fragmentation of neutrophils in the skin lesions from the patients might be due to apoptosis. Inducible nitric oxide synthase and nitrotyrosine were detected in infiltrates, and interleukin-8 was also detected in vascular endothelial cells in those skin lesions. The roles of nitric oxide and interleukin-8 in the apoptosis of neutrophils are discussed. Topics: Adolescent; Adult; Aged; Anaphylaxis; Apoptosis; Cell Nucleus; Child; Child, Preschool; DNA Fragmentation; Endothelium, Vascular; Female; Humans; Interleukin-8; Leukocyte Count; Male; Middle Aged; Neutrophils; Nitric Oxide Synthase; Purpura; Skin Diseases; Tyrosine | 1997 |
Identification of leukotriene B4 as the neutrophil chemotactic factor released by antigen challenge from passively sensitized guinea pig lungs.
Neutrophils are prominent in some IgE-mediated allergic reactions and may contribute to the pathophysiology of immediate hypersensitivity. Antigen challenge of fragments of guinea pig lung tissue that were passively sensitized with IgE or IgG antibody evoked the release of neutrophil chemotactic activity (NCA) in parallel with histamine. The NCA released from lung tissue by both IgG- and IgE-dependent stimulation coeluted from a column of Sephacryl S-300 with synthetic leukotriene B4 (LTB4). The NCA in eluates from the Sephacryl S-300 column contained LTB4, as determined by high-performance liquid chromatography and specific radioimmunoassay, in quantities that accounted for the observed chemoattractant activity in the eluates. Furthermore, the NCA of supernatants from antigen-challenged lung fragments was reduced by a mean of 80% after absorption with a monoclonal antibody to LTB4. LTB4 thus constitutes the major functional constituent of NCA released after anaphylactic challenge of IgE- and IgG-sensitized guinea pig lung tissue. Topics: Anaphylaxis; Animals; Chemotactic Factors; Guinea Pigs; Immunization, Passive; Immunoglobulin E; Immunoglobulin G; Interleukin-8; Leukotriene B4; Lung; Male; Neutrophils; Ovalbumin | 1989 |
Release of neutrophil and eosinophil chemotactic factor from sensitized skin in vitro cutaneous anaphylactic reactions.
Topics: Anaphylaxis; Animals; Cell Movement; Chemotactic Factors; Chemotactic Factors, Eosinophil; Guinea Pigs; Humans; Interleukin-8; Leukotriene B4; Skin | 1989 |
Neutrophil chemotactic factor of anaphylaxis.
Topics: Anaphylaxis; Animals; Asthma, Exercise-Induced; Chemotactic Factors; Forced Expiratory Volume; Guinea Pigs; Histamine Release; Humans; Hyperventilation; Interleukin-8; Mast Cells; Molecular Weight | 1982 |