
IndraLab
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"In the CNS, activation of IL-1R1 by IL-1beta activates signaling pathways that modulate intracellular calcium [XREF_BIBR], expression of neurotransmitter receptors [XREF_BIBR], activation of cAMP response element binding (CREB) [XREF_BIBR] and brain derived neurotrophic factor (BDNF) expression [XREF_BIBR]."
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"Lung infections are influenced by a balance of pro-inflammatory cytokines, such as TNF-α and IL-1β, which promote inflammation, and anti-inflammatory cytokines, including IL-10, TGF-β, and IL-1ra, which are secreted by alveolar macrophages to mitigate the inflammatory response [24]."
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"This notion is supported by our invitro studies, which showed that IL-1beta can induce IL-1Ra production in both transformed INS-1 beta-cells and alphaTC-1 cells; albeit IL-1Ra immunoreactivity was much lower in alphaTC-1 cells and inducing IL-1Ra production in alphaTC-1 cells required a higher concentration of IL-1beta as compared to INS-1 beta-cells."
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"Because IL-1beta has been reported to trigger the IL-1R1 signaling pathway, which activates signaling proteins, such as mitogen activated kinases (c-Jun N-terminal kinase (JNK), p38, extracellular signal regulated kinase (ERK)) and transcription factors (nuclear factor (NF)-kappaB) 35, we analyzed the effects of NF-kappaB inhibitor (Bay11-7082) and p38 inhibitor (SB203580) treatment."
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"There are NF-κB binding sites upstream of the IL-1Ra promoter ; IL-1Ra is reported to be upregulated by IL-1β in endometrial stromal cells ; the expression of IL1Ra follows the expression of IL-1β when induced by LPS in Schwann cells , and both are upregulated in response to leptin in β-cells."
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"In addition, the Fas mediated IL-1beta production was required for Th17 and Th1 induction during bacterial infection : Th17 and Th1 induction was abolished in Fas -/- mice, whereas supplementation with recombinant IL-1beta restored Th17 and Th1 induction via IL-1 receptor 1 (IL-1R1), and rescued the mortality of Fas -/- mice infected with Listeria IL-1R1, but not apoptosis associated speck like protein containing a caspase recruitment domain or Fas on T cells, was required for Th17 and Th1 induction, indicating that IL-1beta stimulates IL-1R1 on T cells for Th17 and Th1 induction."
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"The results show that chronic icy microinfusion of IL-1 beta induced significant anorexia, increased the cerebellar IL-1RI mRNA content, increased IL-1Ra and IL-1 beta mRNAs levels in the cerebellum> midbrain> cortex> hippocampus, and induced profiles of IL-1RI mRNA, IL-1Ra mRNA, and IL-1 beta mRNA that were highly intercorrelated."
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"In cisplatin-induced nephrotoxicity, increased expression of IL-1β was detected, which triggered the activation of IL-1R, inducing TNF-α production and leading to AKI, suggesting that knocking out IL-1 receptor holds the potential of decreasing cisplatin-induced acute kidney injury [57]."
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"Moreover, exercise training increased WBC and lymphocytes numbers at 6 h after LPS exposure (Supplementary Fig. 3f–i), reduced serum levels of the pro-inflammatory cytokines including TNF, IL-1β and TIMP-1, increased the anti-inflammatory cytokine IL-1Ra (Supplementary Fig. 3j–m), mitigated liver, lung and spleen injury caused by LPS challenge (Supplementary Fig. 3n–p)."
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"Together, the similar kinetics of PGE production, PG profiles and the induction of mPGES-1/COX-2 axis suggest that IL-1β /HMGB1 complexes mediate their effects on the prostanoid cascade through the same pathway as IL-1β, via the IL-1RI receptor.Further, we studied whether the induction of the PGE synthesis cascade and the cytokine response by IL-1β /HMGB1 complexes were mediated via IL-1RI using the IL-1Ra."
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"However, IL-1beta alone could not induce IL-17 production in Il1rn -/- gammadelta T cells, even though these cells expressed IL-1R, consistent with a report that IL-1beta alone does not induce IL-17 in peritoneum- and lung derived gammadelta T cells expressing high levels of IL-1R XREF_BIBR."
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"We also show that P. aeruginosa activates NF-κB in macrophages through both the TIR-containing adaptor protein (TIRAP)/MyD88 dependent and the TRIF-dependent pathways, and that IL-1α and IL-1β activation of IL-1R1 is an important feedback pathway in the host response to P. aeruginosa."
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"IL-1RA is an endogenous inhibitor of IL-1R1 ( xref ). xref suggested that IL-1β activates IL-1R1 on neurons and induces tyrosine phosphorylation of the NR2B subunit of NMDA receptor through Src kinase, leading to increased NMDA receptor-mediated calcium influx, thereby enhancing neuronal excitability."
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"Specifically, IL-1β, SDF1α, and VEGF activate G-protein-coupled receptors (GPCRs), receptor tyrosine kinases (RTKs), and TLR/IL-1R, leading to activation of Ras and its downstream target phosphoinositide 3-kinase γ (PI3Kγ), the PI3K isoform predominantly expressed in myeloid cells ."
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"Combining these previous studies with the present findings, a host defense pathway has been discovered whereby neutrophils represent a source of IL-1β, which subsequently activates IL-1R expressed on non-bone marrow-derived resident skin cells to promote effective neutrophil recruitment in host defense during a S. aureus skin infection."
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"In contrast, in a
S. aureus osteomyelitis model, both IL-1β and
IL-1α contributed to the IL-1R/MyD88-mediated host defense , suggesting that the anatomical
location of the S. aureus infection and the presence of the
orthopaedic implant likely contributed to the more predominant host defense role of
IL-1β rather than IL-1α."
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"Microbial products and cytokines interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) acts as primary stimuli and initiates inflammation through interacting with the toll like receptors (TLR)s, IL-1 receptor (IL-1R), IL-6 receptor (IL-6R), and the TNF receptor (TNFR) reported by Kaminska in 2005 (Kaminska, 2005)."
| PMC
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"Additional treatment with conditioned media from SF-UC-MSCs downregulated their gene expression by 0.25-fold, 0.71-fold, 0.80-fold, and 0.29-fold, respectively.With respect to anti-inflammatory cytokines, IL-1β significantly downregulated the gene expressions of IL-4 by 0.48-fold; however, IL-1β upregulated those of IL-10 and IL-1ra by 1.4-fold and 211.1-fold (Figure 3D), respectively."
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"In response to IL-1β, U251 and U87MG GB cell lines secreted more IL-1β and the high IL-1β conditioned media of U87MG promotes angiogenesis and neurotoxicity in human umbilical vein endothelial cells and neurons, respectively. xref It was reported that IL-1β stimulation increased IL-8 and CCL2 secretion in the U251 GB cell line, suggesting monocyte-neutrophil recruitment and proangiogenic environment ( xref ). xref Additionally, a report in a mouse model of GB has shown that monocyte infiltration in TM produces more IL-1β activating IL-1R in GB cells, inducing an interplay between GB and monocytes that promotes tumor progression. xref These reports suggest a crucial circuit between GB and immune cells via IL-1β."
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"A major branch of the innate immune system is regulated by the Toll like receptors (TLRs), which are receptors for endogenous damage associated molecules released from injured cells as well as pathogen derived molecules, and interleukin-1 receptors (IL-1R), which are activated by IL-1alpha, IL-1beta and IL-18 cytokines."
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"IL-1RA, an anti-inflammatory cytokine, is induced by IL-1beta and blocks the pro inflammatory cytokine action of IL-1beta at IL-1 receptor I. IL-1RA can be easily measured compare with IL-1beta, and systemic levels of IL-1RA are elevated in obesity, insulin resistance and type 2 diabetes patients."
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"In addition, it has been shown in mice, albeit not in rats, that the midline raphe nuclei express in IL-1 receptors [XREF_BIBR] and that IL-1beta- and LPS induced increase SERT activity and LPS induced immobility in the tail suspension test, a measure of behavioral despair, were abolished in IL-1R knockout mice [XREF_BIBR]."
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"IL-1beta (the main secreted isoform) is produced by microglia to act primarily on astrocytes, and we have reported previously that IL-1beta induces the production of secondary inflammatory mediators via binding to the IL-1 receptor type 1 (IL-1R1) and downstream activation of the extracellular signal regulated kinase (ERK1/2) in these cells."
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"While IL-1R1 can be stimulated by either of two cytokines, IL-1alpha or IL-1beta, it has been shown that IL-1beta plays a pivotal role in disease pathogenesis because it not only directly stimulates IL-1R1-dependent inflammatory signaling, but is also needed for the secretion of IL-1alpha from cells."
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"Our findings indicate that : (i) IL-1beta directly affects the central nervous system and acts independently of infiltrating hematogenous cells; (ii) IL-1beta induces microglial activation but is not neurotoxic per se; (iii) IL-1beta enhances excitotoxic neuronal damage and microglial activation and (iv) IL-1ra, even when applied for only 4 h, reduces neuronal cell death and the number of microglial cells after excitotoxic damage."
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"Under basal conditions, mIL-1R1 is undetectable and microglia marginally respond to IL-1β.13 In vitro direct stimulation of microglia with LPS can drive IL-1R1 production but mIL-1R1 dependent products were not examined.20 Following LPS preconditioning, newly expressed mIL-1R1 allows microglia to directly respond to subsequent IL-1β administration via change of morphology and production of IL-1 family cytokines."
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"The stimulation of the inflammatory response after MI is significantly influenced by IL-1 signaling: apart from the discharge of IL-1α by necrotic cells, the upregulated type 1 IL-1 receptor (IL-1R1) in respondent leukocytes and fibroblasts is driven by de novo synthesis and activation of IL-1β [11]."
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"Primary sensory neurons particularly nociceptors in DRGs express IL-1 receptors (IL-1R), and activation of IL-1R by IL-1β can activate nociceptors rapidly to generate action potentials and elicit pain hypersensitivity via regulating sodium and potassium currents [ xref , xref ]."
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"Likewise, parallel cultures comparing IL-1R1 hi and IL-1R1 lo subpopulations of stage 3 iNK cells revealed that, whereas IL-15 alone maintained survival of both IL-1R1 hi and IL-1R1 lo subpopulations of stage 3 iNK cells in vitro, the addition of IL-1beta enhanced proliferation of the IL-1R1 hi, but not the IL-1R1 lo, subpopulation of stage 3 iNK cells (XREF_FIG)."
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"Although ACS (IRAP II (TM)) increased IL-1Ra and IGF-1 in equine cartilage explants treated with IL-1beta, there was no significant difference in MMP-3 production and proteoglycan loss or synthesis between ACS and serum treated samples suggesting minimal beneficial effects of ACS on cartilage matrix metabolism."
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"In the CNS, activation of IL-1R1 by IL-1β activates signaling pathways that modulate intracellular calcium [ xref ], expression of neurotransmitter receptors [ xref ], activation of cAMP response element-binding (CREB) [ xref ] and brain-derived neurotrophic factor (BDNF) expression [ xref ]."
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"S. aureus also activates the inflammasome (which has been shown to be in part mediated by S. aureus derived ATP, alpha-toxin, beta-hemolysin, gamma-hemolysin and PVL) that results in proteolytic processing and cellular release of IL-1beta, which activates the IL-1R to induce production of proinflammatory and antimicrobial immune responses against S. aureus."
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"We also show that P. aeruginosa activates NF-kappaB in macrophages through both the TIR containing adaptor protein (TIRAP)/MyD88 dependent and the TRIF dependent pathways, and that IL-1alpha and IL-1beta activation of IL-1R1 is an important feedback pathway in the host response to P. aeruginosa."
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"Next, we emphasize the role of IL-1β and HMGB1 in SE by providing the examples listed below:During recurrent seizures, endogenous “danger signals”, which are activated by potentially pathogenic damage, activate toll-like receptor 4 (TLR4) and brain cells release HMGB1, while IL-1β, released from neurons, glial cells, and brain endothelial cells during inflammasome activation, and macrophages expelled from the blood, activate IL-1R1 in epilepsy [112,116,117]."
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"These include CXCL1/KC and probably CXCL2, 5, and 8, which recruit neutrophils from limbal capillaries to the corneal stroma, and IL-1alpha and IL-1beta, which then feedback to activate the IL-1R1 and MyD88 pathway in macrophages and most likely also in resident corneal epithelial cells and stromal fibroblasts."