Effect of interleukin-1 receptor antagonist on antigen-induced pulmonary responses in guinea pigs

Selig, William M.; Tocker, Joel

doi:10.1016/0014-2999(92)90621-a

Cited by 59 publications

(27 citation statements)

References 22 publications

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“…In recent years, substantial evidence has been accumulated in support of the concept that cytokines are key regulators of the cascade of cellular events associated with airway inflammation in atopic asthma (2,27,(35)(36)(37)(38). In this regard, some studies have demonstrated elevated levels of various cytokines in the bronchoalveolar lavage fluid from asthmatic patients (8-10).…”

Section: Discussionmentioning

confidence: 99%

“…In this regard, some studies have demonstrated elevated levels of various cytokines in the bronchoalveolar lavage fluid from asthmatic patients (8-10). Moreover, recent animal studies have shown that, apart from their potential role in regulating airway inflammation in the allergic state, certain cytokines (notably IL-1␤ and TNF-␣) may also contribute to the associated heightened airway constrictor responsiveness (2,6,25,27). Finally, administration of specific cytokines has been shown to induce impairment of ␤-adrenoceptor-mediated airway relaxation in the isolated guinea pig trachea (26).…”

Section: Discussionmentioning

confidence: 99%

“…In this connection, exogenous administration of TNF-␣ to animals in vivo has been shown to induce bronchial constrictor hyperresponsiveness (6,25), and treatment of isolated guinea pig airways with IL-1 ␤ or TNF-␣ has been found to reduce isoproterenol-mediated relaxation in vitro (26). Moreover, treatment of antigen-sensitized animals with an IL-1 receptor antagonist has been shown to inhibit both their in vivo bronchial hyperreactivity to histamine (2) or substance P (27), as well as the accompanying pulmonary infiltration with leukocytes, including eosinophils and neutrophils (2,27,28). Collectively, these recent observations support the compelling concept that certain proinflammatory cytokines may be directly involved in mediating changes in airway contractility.…”

Section: Introductionmentioning

confidence: 99%

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Mechanism of cytokine-induced modulation of beta-adrenoceptor responsiveness in airway smooth muscle.

Hákonarson

Herrick²,

Serrano³

et al. 1996

J. Clin. Invest.

128

112

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To elucidate the role of specific proinflammatory cytokines in regulating airway responsiveness, we examined the effects and mechanisms of action of IL-1 ␤ , TNF-␣ , and IL-2 on the ␤ -adrenoceptor-and postreceptor-coupled transmembrane signaling mechanisms regulating relaxation in isolated rabbit tracheal smooth muscle (TSM) segments. During half-maximal isometric contraction of the tissues with acetylcholine, relaxation responses to isoproterenol, PGE 2 , and forskolin were separately compared in control (untreated) TSM and tissues incubated for 18 h with IL-1 ␤ (10 ng/ml), TNF-␣ (100 ng/ml), or IL-2 (200 ng/ml). Relative to controls, IL-1 ␤ -and TNF-␣ -treated TSM, but not IL-2-treated tissues, depicted significant attenuation of their maximal relaxation and sensitivity (i.e., Ϫ log dose producing 50% maximal relaxation) to isoproterenol ( P Ͻ 0.001) and PGE 2 ( P Ͻ 0.05); whereas the relaxation responses to direct stimulation of adenylate cyclase with forskolin were similar in the control and cytokine-treated tissues. Further, the attenuated relaxation to isoproterenol and PGE 2 was ablated in the IL-1 ␤ -treated TSM that were pretreated with either the muscarinic M 2 -receptor antagonist, methoctramine (10

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Mechanism of cytokine-induced modulation of beta-adrenoceptor responsiveness in airway smooth muscle.

Hákonarson

Herrick²,

Serrano³

et al. 1996

J. Clin. Invest.

128

112

View full text Add to dashboard Cite

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“…This response is abrogated when the product of the IL-1 receptor antagonist gene, IL-1Ra, competitively binds to the receptor but does not elicit the downstream signal transduction cascade. The pro-inflammatory effect of IL-1 and the antiinflammatory effect of IL-1Ra in asthma have been documented in a number of human and animal studies [9][10][11][12][13].…”

mentioning

confidence: 99%

Interleukin-1R antagonist gene and pre-natal smoke exposure are associated with childhood asthma

Ramadas¹,

Sadeghnejad²,

Karmaus³

et al. 2006

Eur Respir J

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The interleukin-1 receptor antagonist (IL1RN) is a potent anti-inflammatory cytokine. In the present study, association of the human IL1RN gene polymorphisms with asthma, bronchial hyperresponsiveness and forced expiratory volume in one second/forced vital capacity ratio was tested and the data was stratified by environmental tobacco smoke exposure in order to investigate a gene-smoking interaction.In an unselected subset (n5921) of the Isle of Wight birth (UK) cohort, which has previously been evaluated for asthma and related manifestations at ages 1, 2, 4 and 10 yrs, three IL1RN single nucleotide polymorphisms (SNP) were genotyped. Logistic regression and repeated measurement models for tests of association using a representative SNP rs2234678 were used, as all SNPs tested were in strong linkage disequilibrium.In the overall analysis, the SNP rs2234678 was not associated with asthma. However, in the stratum with maternal smoking during pregnancy the rs2234678 GG genotype significantly increased the relative risk of asthma in children, both in analyses of repeated asthma occurrences and persistent asthma.In conclusion, the present results show that in the first decade of life, the gene-environment interaction of the interleukin-1 receptor antagonist gene polymorphism rs2234678 and maternal smoking during pregnancy increased the risk for childhood asthma.

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“…Experimentally, MoAbs to IL-5 have been shown to inhibit disease in guinea pigs [65,66], as has a naturally occurring antagonist of IL-IR, if less so [67]. Direct blockade of adhesion by targeting ICAM-1 has also been attempted with some effect [68].…”

Section: New Therapeutic Strategiesmentioning

confidence: 99%

Therapeutic advances in immunosuppression

Thomson

Forrester

1994

Clinical and Experimental Immunology

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SUMMARYImmunosuppressive therapy is appropriate for the prevention or reversal of allograft rejection, and for the treatment of autoimmune disorders and allergic disease. Recent advances in our understanding of the cellular and molecular mechanisms that regulate immune responses have paralleled elucidation of the modes of action of a variety of therapeutic immunosuppressive agents, both 'old' and new. These developments have identified potential targets for more refined and specific intervention strategies that are now being tested in the clinic.

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Effect of interleukin-1 receptor antagonist on antigen-induced pulmonary responses in guinea pigs

Cited by 59 publications

References 22 publications

Mechanism of cytokine-induced modulation of beta-adrenoceptor responsiveness in airway smooth muscle.

Mechanism of cytokine-induced modulation of beta-adrenoceptor responsiveness in airway smooth muscle.

Interleukin-1R antagonist gene and pre-natal smoke exposure are associated with childhood asthma

Therapeutic advances in immunosuppression

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