Disease relevance of Il13

• The CNS transcription of the HIV-1 replication factor IL-1beta in the context of limited transcription of the IL-1 replication inhibitors IL-1ra, IL-10, and IL-13 might help explain the negative impact of systemic inflammation on the clinical course of AIDS [1].
• Our data strongly suggest that IL-13 may control brain inflammation by inducing the death of activated microglia in vivo, resulting in an enhancement of neuronal survival [2].
• Using a reverse transcriptase-polymerase chain reaction method, a cDNA for the complete coding region and part of the 5'-untranslated region of rat IL-13 was cloned from rat renal cortex RNA following the induction of anti-glomerular basement membrane antibody-induced glomerulonephritis [3].
• Furthermore, LPS- and OX8-stimulated AM from Brown Norway rats produce more Th2 type cytokines (IL-10 and IL-13) than AM from Sprague Dawley rats, suggesting that these cells may play an important role in creating a cytokine milieu that may favour the development of allergic reactions [4].
• This represents a potential mechanism by which IL-4/IL-13 could play a role in the pathogenesis of lung fibrosis [5].

High impact information on Il13

• Th2 cells produce cytokines (IL-4, IL-10 and IL-13) that are crucial for control of extracellular helminthic infections and promote atopic and allergic diseases [6].
• IL-10 and IL-13 have powerful antiinflammatory activities in vitro and in vivo [7].
• In the IgG immune complex model of lung injury in rats, exogenously administered IL-10 or IL-13 have recently been shown to suppress neutrophil recruitment and ensuing lung injury by greatly depressing pulmonary production of TNF alpha [7].
• Interleukin (IL) 1beta, IL-1 receptor antagonist, IL-10, and IL-13 gene expression in the central nervous system and anterior pituitary during systemic inflammation: pathophysiological implications [1].
• Rat KC were activated in vitro with lipopolysaccharide (LPS), and expression of IL-10 mRNA compared with IL-13 and IL-1beta by reverse-transcription polymerase chain reaction (RT-PCR) [8].

Chemical compound and disease context of Il13

• Regulation of found in inflammatory zone 1 expression in bleomycin-induced lung fibrosis: role of IL-4/IL-13 and mediation via STAT-6 [5].
• Real-time, image-guided, convection-enhanced delivery of interleukin 13 bound to pseudomonas exotoxin [9].

Biological context of Il13

• In conclusion, cytoprotection rendered by virally induced IL-13 against hepatic I/R injury in this clinically relevant rat hepatic cold I/R injury model was accomplished via decreased apoptosis and induction of antiapoptotic/antioxidant molecules [10].
• Microglia expressing interleukin-13 undergo cell death and contribute to neuronal survival in vivo [2].
• The deduced amino acid sequence of rat IL-13 reveals 63% and 79% homology with the human and mouse proteins, respectively [3].
• These data indicate that endogenous IL-10, IL-13 and SLPI are important regulators of the inflammatory response by reducing gene activation with resultant generation of peptide mediators/cytokines and chemokines [11].
• IL-10 was able to inhibit KC production of both SO and TNF- in vitro, and this was achieved more effectively than IL-4 or IL-13; no such effects were seen on KC phagocytosis [8].

Anatomical context of Il13

• We previously reported that IL-13, an anti-inflammatory cytokine, induced the death of activated microglia [12].
• Both CD4+ and CD8+ T cells are activated in response to allergen challenge in the sensitized rat and express Thelper2 cytokines (IL-4, IL-5 and IL-13) [13].
• Electrophoretic mobility shift analysis of nuclear extracts from alveolar macrophages and whole lung tissues demonstrated that both IL-10 and IL-13 suppressed nuclear localization of NF-kappa B after in vivo deposition of IgG immune complexes [7].
• The present study underlines the importance of IL-10 and IL-13, cytokines with potent antiinflammatory properties, in inhibiting the proinflammatory cytokine (TNF-alpha and IL-1beta)-mediated degradation of SM to ceramide in rat primary astrocytes [14].
• To identify the active component involved, we examined the expression of known macrophage deactivators IL-10, IL-13, and TGF-beta 1 in mesangial cells [15].

Associations of Il13 with chemical compounds

• We found that COX-2 inhibitors (celecoxib and NS398) suppressed the death of microglia induced by a combination of LPS and IL-13 and that exogenous addition of PGE(2) and 15d-PGJ(2) induced microglial death [12].
• Agonists of EP2 (butaprost) and peroxisome proliferator-activated receptor gamma (ciglitazone) mimicked the effect of PGE(2) and 15d-PGJ(2), and an EP2 antagonist (AH6809) and a peroxisome proliferator-activated receptor gamma antagonist (GW9662) suppressed microglial death induced by LPS in combination with IL-13 [12].
• Interleukin-10 and interleukin-13 inhibit proinflammatory cytokine-induced ceramide production through the activation of phosphatidylinositol 3-kinase [14].
• In the present report, we show that injection of lipopolysaccharide (LPS) into the rat cortex led to increased levels of interleukin-13 (IL-13) and to IL-13 immunoreactivity, followed by the substantial loss of microglia at 3 days post-LPS [2].
• Octreotide reduced IL-12 (P < 0.05) and increased IL-13 (P < 0.05) production by unstimulated KC [16].

Regulatory relationships of Il13

• Interleukin-13 enhances cyclooxygenase-2 expression in activated rat brain microglia: implications for death of activated microglia [12].
• These findings indicate that IL-13 induces CCSP expression via an EGFR- and leukocyte-dependent pathway [17].
• IL-4 and IL-13 upregulate arginase I expression by cAMP and JAK/STAT6 pathways in vascular smooth muscle cells [18].

Other interactions of Il13

• In vivo suppression of NF-kappa B and preservation of I kappa B alpha by interleukin-10 and interleukin-13 [7].
• However, inhibition of HO-1 with tin protoporphyrin reversed cytoprotective/antiapoptotic effects of IL-13 [10].
• Treatment of rat primary astrocytes with TNF-alpha or IL-1beta led to rapid degradation of SM to ceramide, whereas IL-10 and IL-13 by themselves were unable to induce the degradation of SM to ceramide [14].
• Under the basal culture conditions, strong expression of TGF-beta 1 mRNA was observed, whereas expression of neither IL-10 nor IL-13 was detected [15].
• There was no marked change in IL-5, IL-13 or transforming growth factor-beta (TGF-beta) in either strain [19].

Analytical, diagnostic and therapeutic context of Il13

• Northern blot analysis of lung mRNA showed that, in the presence of IgG immune complexes, IL-10 and IL-13 augmented I kappa B alpha mRNA expression [7].
• Cytoprotective and antiapoptotic effects of IL-13 in hepatic cold ischemia/reperfusion injury are heme oxygenase-1 dependent [10].
• The production of TNFalpha, IL-6, IL-10, IL-12 and IL-13 was assessed in culture supernatants by ELISA and that of nitric oxide (NO) by a modification of the Griess reaction [16].
• However, expressions of Th2 cytokines (IL-4, IL-10, and IL-13) induced by e-PTFE were generally higher than those of PDCM and control groups at all times (Mann-Whitney U test, p < 0.05) [20].
• Heme oxygenase 1 mediates the immunomodulatory and antiapoptotic effects of interleukin 13 gene therapy in vivo and in vitro [21].

References