The Emerging Role of Interleukin-1β in Autoinflammatory Diseases

Lane, Thirusha; Lachmann, HJ

doi:10.1007/s11882-011-0207-6

Cited by 32 publications

(24 citation statements)

References 75 publications

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“…It is known that monosodium urate crystals engulfed by phagocytes cause an intracellular electrolyte disturbance that provokes inflammasome activation with subsequent release of cytokines, notably interleukin-1β (IL-1β) 7. The clinical presentation of our case is similar to that observed in autoinflammatory syndromes mediated by IL-1β which are characterised by recurrent episodes of fever, disorientation and leucocytosis affecting the joints, skin and serosal surfaces 8. Moreover, the release of cytokines stimulates endothelial cells, leading to vasodilatation, increased permeability to plasma proteins and the recruitment of leukocytes into tissues 9…”

Section: Discussionsupporting

confidence: 61%

Severe systemic inflammatory response syndrome immediately after spinal surgery in a patient with axial gout

et al. 2018

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We report a 55-year-old man with gouty arthritis who developed a 3-month history of low back pain, gradual lower extremities weakness and urinary incontinence. Lumbar MRI showed an exophytic lesion at L3-L4. Immediately after spinal decompression surgery, he developed fever, disorientation, polyarthritis, acute kidney injury and leucocytosis. He was treated with multiple antimicrobial agents for presumed spinal abscess but did not improve. Multiple body site cultures were negative. Aspiration of the sacroiliac joint revealed the presence of monosodium uric acid crystals. A diagnosis of acute gout was done, and he was treated with high-dose intravenous methylprednisolone and colchicine. Within 48 hours, he had a remarkable clinical improvement. At discharge, neurological and laboratory abnormalities had resolved. Awareness of risk factors for axial gout and a high degree of suspicion are important to establish a prompt diagnosis and treatment to prevent severe complications as seen in this case.

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Section: Discussionsupporting

confidence: 61%

Severe systemic inflammatory response syndrome immediately after spinal surgery in a patient with axial gout

et al. 2018

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“…Having established that LPS induced widespread changes in the expression of lncRNAs and eRNAs in human monocytes that were located close to differentially expressed inflammatory genes, it was important to determine whether these were of functional relevance. Of particular interest for regulation of the innate immune response, was our identification of multiple non-coding transcripts that are situated close to the IL1β gene, an important cytokine that stimulates inflammatory responses in multiple cell types and whose overproduction has been implicated in autoimmune diseases2841. These included a downstream eRNA ( eRNA-IL1β-eRNA ) and an upstream mRNA-flanking RBT ( IL1β-RBT46 ).…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNAs and enhancer RNAs regulate the lipopolysaccharide-induced inflammatory response in human monocytes

et al. 2014

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Early reports indicate that long non-coding RNAs (lncRNAs) are novel regulators of biological responses. However, their role in the human innate immune response, which provides the initial defence against infection, is largely unexplored. To address this issue, here we characterize the long non-coding RNA transcriptome in primary human monocytes using RNA sequencing. We identify 76 enhancer RNAs (eRNAs), 40 canonical lncRNAs, 65 antisense lncRNAs and 35 regions of bidirectional transcription (RBT) that are differentially expressed in response to bacterial lipopolysaccharide (LPS). Crucially, we demonstrate that knockdown of nuclear-localized, NF-κB-regulated, eRNAs (IL1β-eRNA) and RBT (IL1β-RBT46) surrounding the IL1β locus, attenuates LPS-induced messenger RNA transcription and release of the proinflammatory mediators, IL1β and CXCL8. We predict that lncRNAs can be important regulators of the human innate immune response.

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“…The overproduction of proinflammatory mediators and cytokines by activated macrophages causes various inflammatory diseases (Tsatsanis et al 2006;Keystone and Ware 2010;Lane and Lachmann 2011;Kalinski 2012;Rossi et al 2015). Therefore, identifying new agents capable of lowering proinflammatory reactions are essential for the alleviation of a number of inflammation-related disorders attributed to macrophage activation.…”

Section: Discussionmentioning

confidence: 99%

“…The activated macrophages secrete proinflammatory mediators, such as nitric oxide (NO) and prostaglandin E 2 (PGE 2 ), which are synthesized by inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2), respectively (Tsatsanis et al 2006;Kalinski 2012). They also produce inflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β (Keystone and Ware 2010;Lane and Lachmann 2011;Lee et al 2015;Rossi et al 2015). Therefore, the inhibition of macrophage activation has been suggested as a potential therapeutic goal in relieving the progression of inflammatory diseases.…”

Section: Introductionmentioning

confidence: 99%

Fructus sophorae attenuates secretion of proinflammatory mediators and cytokines through the modulation of NF-κB and MAPK signaling pathways in LPS-stimulated RAW 264.7 macrophages

Choi

Kang²

2016

gpb

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Abstract. This study investigated the inhibitory effects and underlying mechanisms of Fructus sophorae, the dried ripe fruit of Styphnolobium japonicum (L.) Schott, on the production of proinflammatory molecules in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. The results indicated that pretreatment with noncytotoxic concentrations of Fructus sophorae extract (FSE) significantly inhibited the release of the proinflammatory mediators nitric oxide (NO) and prostaglandin E 2 , which were associated with the downregulation of both mRNA and protein for inducible NO synthase and cyclooxygenase-2, respectively, in LPS-challenged RAW 264.7 cells. FSE also blocked the LPS-induced expression of the proinflammatory cytokines interleukin (IL)-6 and IL-1β. Furthermore, the results showed that FSE efficiently attenuated the LPS-induced nuclear translocation of nuclear factor-kappa B (NF-κB) and phosphorylation of the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) but not p38 MAPK. These results suggest that FSE exhibits anti-inflammatory activity by inhibiting proinflammatory mediators and cytokines through the inactivation of NF-κB, ERK and JNK, and it may offer therapeutic potential for treating inflammatory diseases accompanied with macrophage activation.

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The Emerging Role of Interleukin-1β in Autoinflammatory Diseases

Cited by 32 publications

References 75 publications

Severe systemic inflammatory response syndrome immediately after spinal surgery in a patient with axial gout

Severe systemic inflammatory response syndrome immediately after spinal surgery in a patient with axial gout

Long non-coding RNAs and enhancer RNAs regulate the lipopolysaccharide-induced inflammatory response in human monocytes

Fructus sophorae attenuates secretion of proinflammatory mediators and cytokines through the modulation of NF-κB and MAPK signaling pathways in LPS-stimulated RAW 264.7 macrophages

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