IndraLab
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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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"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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"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."
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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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"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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"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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"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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"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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"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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"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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"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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"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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"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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"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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"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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"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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"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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"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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"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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"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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"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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"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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"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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"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 ]."