Recombinant interleukin-1 receptor antagonist blocks the proinflammatory activity of endogenous interleukin-1 in rabbit immune colitis

Cominelli, Fabio; Nast, Cynthia C.; Duchini, Andrea; Lee, Marjorie

doi:10.1016/0016-5085(92)91096-m

Cited by 178 publications

(89 citation statements)

References 33 publications

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“…These data support a possible role of IL-1␤ in the pathogenesis of ulcerative colitis. This notion is further supported by the data obtained from animal models showing that administration of IL-1ra attenuates rabbit immune complex colitis (Cominelli et al, 1992) and reduction of IL-1ra levels in gene knockout mice (Hirsch et al, 1996) and by antibody neutralization in rabbits (Ferretti et al, 1994) increases the susceptibility to the induction of experimental colitis.…”

mentioning

confidence: 69%

Interleukin 1β-Induced Production of H₂O₂Contributes to Reduced Sigmoid Colonic Circular Smooth Muscle Contractility in Ulcerative Colitis

Cao¹,

Vrees²,

Potenti³

et al. 2004

J Pharmacol Exp Ther

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We have shown that neurokinin A-induced contraction of human sigmoid circular muscle (HSCM) is reduced in patients with ulcerative colitis and that interleukin (IL)-1␤ may play a role in this change. We now examine changes in the signal transduction pathway mediating neurokinin A-induced contraction of HSCM and explore the role of IL-1␤ and of H 2 O 2 in these changes. In Fura 2-AM-loaded ulcerative colitis HSCM cells, neurokinin A-and caffeine-induced peak Ca 2ϩ increase and cell shortening were significantly reduced. In normal cells, neurokinin A-induced contraction was decreased by protein kinase

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mentioning

confidence: 69%

Interleukin 1β-Induced Production of H₂O₂Contributes to Reduced Sigmoid Colonic Circular Smooth Muscle Contractility in Ulcerative Colitis

Cao¹,

Vrees²,

Potenti³

et al. 2004

J Pharmacol Exp Ther

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“…Taken together, our results imply that pyroptotic CD11b + -derived IL-1b is responsible for TH1-mediated colitis progression in our model. Previously, administration of IL-1Ra has also proved to be anti-inflammatory in a model of acute immune-complex colitis in rabbits (52). However, genetic studies using caspase-1 2/2 (47, 53) and IL-1R1 2/2 mice (54) rather implied a protective role for the inflammasome and related IL-1b signaling in acute DSS colitis in mice.…”

Section: Discussionmentioning

confidence: 99%

Loss of TLR2 Worsens Spontaneous Colitis in MDR1A Deficiency through Commensally Induced Pyroptosis

Eyking

Klepak

et al. 2013

The Journal of Immunology

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Variants of the multidrug resistance gene (MDR1/ABCB1) have been associated with increased susceptibility to severe ulcerative colitis (UC). In this study, we investigated the role of TLR/IL-1R signaling pathways including the common adaptor MyD88 in the pathogenesis of chronic colonic inflammation in MDR1A deficiency. Double- or triple-null mice lacking TLR2, MD-2, MyD88, and MDR1A were generated in the FVB/N background. Deletion of TLR2 in MDR1A deficiency resulted in fulminant pancolitis with early expansion of CD11b+ myeloid cells and rapid shift toward TH1-dominant immune responses in the lamina propria. Colitis exacerbation in TLR2/MDR1A double-knockout mice required the unaltered commensal microbiota and the LPS coreceptor MD-2. Blockade of IL-1β activity by treatment with IL-1R antagonist (IL-1Ra; Anakinra) inhibited colitis acceleration in TLR2/MDR1A double deficiency; intestinal CD11b+Ly6C+-derived IL-1β production and inflammation entirely depended on MyD88. TLR2/MDR1A double-knockout CD11b+ myeloid cells expressed MD-2/TLR4 and hyperresponded to nonpathogenic Escherichia coli or LPS with reactive oxygen species production and caspase-1 activation, leading to excessive cell death and release of proinflammatory IL-1β, consistent with pyroptosis. Inhibition of reactive oxygen species–mediated lysosome degradation suppressed LPS hyperresponsiveness. Finally, active UC in patients carrying the TLR2-R753Q and MDR1-C3435T polymorphisms was associated with increased nuclear expression of caspase-1 protein and cell death in areas of acute inflammation, compared with active UC patients without these variants. In conclusion, we show that the combined defect of two UC susceptibility genes, MDR1A and TLR2, sets the stage for spontaneous and uncontrolled colitis progression through MD-2 and IL-1R signaling via MyD88, and we identify commensally induced pyroptosis as a potential innate immune effector in severe UC pathogenesis.

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“…These cytokines can increase the activity of the immune cells involved in the inflammation process. The inhibition of interleukine-1-beta activity causes colon infection in rabbits (Cominelli et al, 1992). Furthermore, interleukine-1 can control inflammation by increasing the blood vessel permeability of vessels and speed up the movement of immune factors (Kesavulu et al, 2000).…”

Section: Interleukin-1 and Interferon Gamma Gene Expressionmentioning

confidence: 99%

Effects of Thymoquinone on Interleukin-1 and Interferon Gamma Gene Expression and Antibody Titers against Newcastle Disease in Broiler Chickens under Oxidative Stress

Rastad

Sadeghi

Chamani

et al. 2016

Rev. Bras. Cienc. Avic.

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KeywordsBroiler, interferon gamma, interleukine-1, thymoquinone, tert-butyl hydroperoxide.Submitted: December/2015 Approved: June/2016 ABStRACtAn experiment was conducted to determine the effects of the dietary inclusion of different levels of thymoquinone (TQ) of broilers subjected to oxidative stress or not on the antibody titers against Newcastle disease and on the gene expression of interleukine-1 and interferon gamma. A total of 320 one-day-old broilers was randomly assigned to eight treatments with four replicates of 10 birds each, in a 4 × 2 factorial arrangement, consisting of four thymoquinone (TQ) levels (0, 5, 8, or 11 mg/kg body weight) and two levels tert-butyl hydroperoxide (t-BHP) injection (0 or 0.02 mmol/kg of body weight). Blood samples were collected from two birds per replicate to determine antibody titers against Newcastle disease. At the end of experiment, two birds per replicate were randomly selected, sacrificed and their spleens were collected to evaluate the genes expressioninterleukin-1 and interferon gamma (p<0.05). The dietary inclusion of TQ of broilers subjected or not oxidative stress increased antibody production against Newcastle disease (p<0.05). Both individual and combined dietary inclusion of t-BHP and TQ promote the differentiation and proliferation of spleen cells and the gene expression of interleukin-1 and interferon gamma (p<0.05).

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Recombinant interleukin-1 receptor antagonist blocks the proinflammatory activity of endogenous interleukin-1 in rabbit immune colitis

Cited by 178 publications

References 33 publications

Interleukin 1β-Induced Production of H₂O₂Contributes to Reduced Sigmoid Colonic Circular Smooth Muscle Contractility in Ulcerative Colitis

Interleukin 1β-Induced Production of H₂O₂Contributes to Reduced Sigmoid Colonic Circular Smooth Muscle Contractility in Ulcerative Colitis

Loss of TLR2 Worsens Spontaneous Colitis in MDR1A Deficiency through Commensally Induced Pyroptosis

Effects of Thymoquinone on Interleukin-1 and Interferon Gamma Gene Expression and Antibody Titers against Newcastle Disease in Broiler Chickens under Oxidative Stress

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Recombinant interleukin-1 receptor antagonist blocks the proinflammatory activity of endogenous interleukin-1 in rabbit immune colitis

Cited by 178 publications

References 33 publications

Interleukin 1β-Induced Production of H2O2Contributes to Reduced Sigmoid Colonic Circular Smooth Muscle Contractility in Ulcerative Colitis

Interleukin 1β-Induced Production of H2O2Contributes to Reduced Sigmoid Colonic Circular Smooth Muscle Contractility in Ulcerative Colitis

Loss of TLR2 Worsens Spontaneous Colitis in MDR1A Deficiency through Commensally Induced Pyroptosis

Effects of Thymoquinone on Interleukin-1 and Interferon Gamma Gene Expression and Antibody Titers against Newcastle Disease in Broiler Chickens under Oxidative Stress

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Interleukin 1β-Induced Production of H₂O₂Contributes to Reduced Sigmoid Colonic Circular Smooth Muscle Contractility in Ulcerative Colitis

Interleukin 1β-Induced Production of H₂O₂Contributes to Reduced Sigmoid Colonic Circular Smooth Muscle Contractility in Ulcerative Colitis