Search results for "IL-13"

showing 5 items of 5 documents

IL-13 and IL-33 Serum Levels Are Increased in Systemic Sclerosis Patients With Interstitial Lung Disease

2022

ObjectiveSystemic sclerosis (SSc) mortality is extremely variable in its internal organ involvement. Pulmonary fibrosis occurs in up to 30% of the cases. Animal models provide evidence that IL-33 is able to induce both cutaneous and pulmonary fibrosis via increased IL-13 and in SSc patients the levels of IL-33 correlate with skin fibrosis. Our aim was to test whether both IL-33 and IL-13 are higher in patients with diffuse SSc and interstitial lung disease (SSc-ILD) compared to SSc patients without ILD and healthy controls.MethodsSerum levels of IL-13 and IL-33 were measured in 30 SSc patients with diffuse disease and 30 healthy controls by enzyme-linked immunosorbent assay. The extent of p…

interstitial lung diseaseMedicine (General)R5-920interleukinsintegumentary systemsystemic sclerosisIL-13IL-13; IL-33; interleukins; interstitial lung disease; systemic sclerosisIL-33General Medicinerespiratory systemskin and connective tissue diseases
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TNFSF14 (LIGHT) Exhibits Inflammatory Activities in Lung Fibroblasts Complementary to IL-13 and TGF-β

2018

The cytokine TNFSF14 [homologous to Lymphotoxin, exhibits Inducible expression and competes with HSV Glycoprotein D for binding to HVEM, a receptor expressed on T lymphocytes (LIGHT)] has been shown in mouse models to be important for development of lung tissue remodeling that is characteristic of asthma, idiopathic pulmonary fibrosis (IPF), and systemic sclerosis (SSc). However, its cellular targets are not fully delineated. In the present report, we show that LTβR and HVEM, the receptors for LIGHT, are constitutively expressed in primary human lung fibroblasts (HLFs). We asked whether LIGHT could promote inflammatory and remodeling-relevant activity in HLFs and how this was similar to, or…

0301 basic medicinelcsh:Immunologic diseases. AllergyTGF-βChemokineTumor Necrosis Factor Ligand Superfamily Member 14medicine.medical_treatmentImmunologyGene ExpressionInflammationProinflammatory cytokineCell Line03 medical and health sciences0302 clinical medicineTransforming Growth Factor betamedicineImmunology and AllergyHumansLungCells CulturedOriginal ResearchCell ProliferationInterleukin-13biologyChemistrylung fibroblastsasthmaFibroblasts3. Good healtha receptor expressed on T lymphocytes030104 developmental biologyCytokineLymphotoxinCXCL5030220 oncology & carcinogenesisIL-13Interleukin 13biology.proteinCancer researchCytokinesexhibits Inducible expression and competes with HSV Glycoprotein D for binding to HVEMmedicine.symptomhomologous to LymphotoxinInflammation Mediatorslcsh:RC581-607MyofibroblastBiomarkersFrontiers in Immunology
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RUOLO DELL’IL-13 NELLA DESENSIBILIZZAZIONE DEL RECETTORE beta2 ADRENERGICO NELLE CELLULE EPITELIALI BRONCHIALI PRIMARIE UMANE

2014

IL-13 induced beta2-adrenergic receptor (ß2-AR) desensitization in human airway epithelial cells.

IL-13 recettore beta due adrenergico cellule epiteliali bronchialiIL-13 beta2-adrenergic receptor human airway epithelial cells.
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Interleukin 13 (IL-13)-regulated expression of the chondroprotective metalloproteinase ADAM15 is reduced in aging cartilage

2020

Objective The adamalysin metalloproteinase 15 (ADAM15) has been shown to protect against development of osteoarthritis in mice. Here, we have investigated factors that control ADAM15 levels in cartilage. Design Secretomes from wild-type and Adam15−/− chondrocytes were compared by label-free quantitative mass spectrometry. mRNA was isolated from murine knee joints, either with or without surgical induction of osteoarthritis on male C57BL/6 mice, and the expression of Adam15 and other related genes quantified by RT-qPCR. ADAM15 in human normal and osteoarthritic cartilage was investigated similarly and by fluorescent immunohistochemistry. Cultured HTB94 chondrosarcoma cells were treated with …

Senescencemedicine.medical_specialtyADAM15medicine.medical_treatmentOsteoarthritisDiseases of the musculoskeletal systemArticleMetalloproteaseAgeSettore BIO/13 - Biologia ApplicataInternal medicineOsteoarthritismedicineddc:610MetalloproteinaseMetalloproteinaseADAM15ChemistryCartilageAutophagyGeneral Medicinemedicine.diseasemedicine.anatomical_structureEndocrinologyCytokineRC925-935IL-13Interleukin 13OsteoarthritiOsteoarthritis and Cartilage Open
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Induction of a disintegrin and metalloprotease 33 during embryonic lung development and the influence of IL-13 or maternal allergy.

2009

Background Asthma pathogenesis involves gene and environmental interactions. A disintegrin and metalloprotease 33 (ADAM33)/Adam33 is a susceptibility gene for asthma and bronchial hyperresponsiveness in human beings and mice. ADAM33 is almost exclusively expressed in mesenchymal cells, including mesenchymal progenitors in developing lungs. Objective Because maternal allergy is a risk factor for asthma, we hypothesized that an allergic environment affects ADAM33/Adam33 expression during human and mouse lung development. Methods Human embryonic/fetal lung (HEL) tissues were collected from first-trimester terminations of pregnancy. These were processed immediately or used for explant culture ±…

OvalbuminImmunologyADAM33AndrologyMiceOrgan Culture TechniquesGene interactionmedicineHypersensitivityImmunology and AllergyAnimalsHumansProtein IsoformsRNA MessengerLungFetusInterleukin-13medicine.diagnostic_testbiologyGene Expression Regulation Developmentalrespiratory tract diseasesOvalbuminADAM ProteinsBronchoalveolar lavageReal-time polymerase chain reactionInterleukin 13Immunologybiology.proteinLung morphogenesisADAM33 IL-13 Asthma AllergyThe Journal of allergy and clinical immunology
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