Gamma-interferon modifies guinea pig airway functions in vitro

H, Chen; Munakata, Mitsuru; Amishima, Masaru; Ukita, Hideaki; Masaki, Yoshihiro; Homma, Yukihiko; Kawakami, Yoshikazu

doi:10.1183/09031936.94.07010074

Cited by 20 publications

(15 citation statements)

References 19 publications

(28 reference statements)

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“…IFN-c enhances LTD 4 -induced contraction in human ASM cells 115 and ASM sensitivity to isoproterenol in guinea pig ASM. 116 In contrast, Hakonarson et al 65 showed that IFN-c prevents asthmatic serumeinduced alterations in ASM responsiveness to either acetylcholine or isoproterenol. Although the JAK/STAT1 pathway is usually the primary component of the IFN-c signaling cascade, Tliba et al 117 recently showed for the first time that TNF-a, via the autocrine activation of IFN-b receptoreassociated JAK1 and Tyk2, stimulates STAT1-dependent and STAT2-dependent gene expression in human ASM cells.…”

Section: Autocrine Effect Of Asm-derived Ifn-bmentioning

confidence: 94%

Synthetic responses in airway smooth muscle

Howarth

Knox²,

Amrani³

et al. 2004

Journal of Allergy and Clinical Immunology

147

105

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Section: Autocrine Effect Of Asm-derived Ifn-bmentioning

confidence: 94%

Synthetic responses in airway smooth muscle

Howarth

Knox²,

Amrani³

et al. 2004

Journal of Allergy and Clinical Immunology

147

105

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“…IFN-␥ may have direct effects on AHR by acting on airway smooth muscle. IFN-␥ was shown to inhibit airway smooth muscle contraction to carbachol, KCl, and TGF-␤ with isoproterenol (39,40) and to inhibit the proliferation of airway smooth muscle (41). Moreover, several studies have reported that intranasal administration of IFN-␥ effectively inhibited goblet cell metaplasia and AHR in a mouse model (34,35,42).…”

Section: Discussionmentioning

confidence: 99%

RANTES (CCL5) Regulates Airway Responsiveness after Repeated Allergen Challenge

Koya

Takeda

Kodama

et al. 2006

Am J Respir Cell Mol Biol

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RANTES (CC chemokine ligand 5) contributes to airway inflammation through accumulation of eosinophils, but the exact role of RANTES (CCL5) is not defined. C57BL/6 mice, sensitized by injection of ovalbumin (OVA) on Days 1 and 14, were challenged with OVA on Days 28, 29, and 30 (3 challenges, short-term-challenge model) or on Days 28, 29, 30, 36, 40, 44, and 48 (7 challenges, repeatedchallenge model) and evaluated 48 h later. Anti-mouse RANTES was given intravenously, and recombinant mouse RANTES or PBS was given intratracheally. These reagents were given on Days 28, 29, and 30 in the short-term-challenge study and on Days 44 and 48 in the repeated-challenge study. After short-term challenge, there were no effects after administration of anti-RANTES or RANTES. In the repeated-challenge study, although control mice showed a decrease in airway hyperresponsiveness, administration of anti-RANTES sustained and enhanced airway hyperresponsiveness and increased goblet cell numbers. In contrast, administration of RANTES normalized airway function but reduced goblet cell numbers. IL-12 and IFN-␥ levels in BAL decreased in the anti-RANTES group and increased in the RANTES group. IFN-␥-producing CD4 T cells in lung, and IFN-␥ production from lung T cells in response to OVA in the anti-RANTES group, were significantly decreased but were increased in the RANTES group. Anti-IFN-␥, administered with RANTES, decreased the effects of RANTES on AHR after repeated challenge. These data indicate that RANTES plays a role in the regulation of airway function after repeated allergen challenge, in part through modulation of levels of IFN-␥ and IL-12. Keywords: airway hyperresponsiveness; IFN-␥; IL-12; RANTES (CCL5)Bronchial asthma is a chronic inflammatory airway disease with the features of reversible airway obstruction and nonspecific airway hyperresponsiveness (AHR). Elevated serum IgE levels and inflammatory cell infiltration, especially of eosinophils, mast cells, and CD4ϩ T cells, seems to be involved in the pathogenesis of the disease (1-3). In animal models of acute allergic inflammation, Th2-cell-derived cytokines, notably IL-4, IL-5, IL-9, and IL-13 and C-C chemokine family members such as RANTES (regulated upon activation, normal T-cell expressed and secreted) and eotaxin-1, are thought to play important roles in the induction of eosinophilic airway inflammation, antigen-specific IgE production, and AHR (4). Although airway inflammation and Th2 cytokines and chemokines are a cornerstone of asthma, the asthmatic response is complex, and the relative importance of some of these contributors may vary with stage or duration of disease.RANTES (CCL5) belongs to the CC chemokine family and induces leukocyte migration by binding to specific receptors in (Received in original form October 19, 2005 and in final form February 16, 2006 ) This work was supported by NIH grants HL-36577 and HL-61005 and EPA grant R825702.Correspondence and requests for reprints should be addressed to Erwin W. Gelfand, M.D., Department of Pediatrics, Nati...

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“…Exposure of tracheal rings obtained from guinea pig (20,135) and mice (161) and isolated smooth muscle cells (4) to inflammatory cytokines resulted in modulation of the responsiveness of airway smooth muscle to a variety of contractile and relaxant agents. Because calcium is a common second messenger molecule for a variety of contractile agonists in airway smooth muscle, we determined the effect of these cytokines on the intracellular calcium responses.…”

Section: Role Of Cd38/cadpr Signaling In Ahrmentioning

confidence: 99%

CD38/cyclic ADP-ribose signaling: role in the regulation of calcium homeostasis in airway smooth muscle

Deshpande¹,

White²,

Doğan³

et al. 2005

American Journal of Physiology-Lung Cellular and Molecular Phys

106

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. CD38/cyclic ADP-ribose signaling: role in the regulation of calcium homeostasis in airway smooth muscle. Am J Physiol Lung Cell Mol Physiol 288: L773-L788, 2005; doi:10.1152/ ajplung.00217.2004.-The contractility of airway smooth muscle cells is dependent on dynamic changes in the concentration of intracellular calcium. Signaling molecules such as inositol 1,4,5-trisphosphate and cyclic ADP-ribose play pivotal roles in the control of intracellular calcium concentration. Alterations in the processes involved in the regulation of intracellular calcium concentration contribute to the pathogenesis of airway diseases such as asthma. Recent studies have identified cyclic ADP-ribose as a calcium-mobilizing second messenger in airway smooth muscle cells, and modulation of the pathway involved in its metabolism results in altered calcium homeostasis and may contribute to airway hyperresponsiveness. In this review, we describe the basic mechanisms underlying the dynamics of calcium regulation and the role of CD38/cADPR, a novel pathway, in the context of airway smooth muscle function and its contribution to airway diseases such as asthma. ryanodine receptor; calcium oscillations; inflammatory cytokines; muscarinic receptors; 12.6-kDa FK506-binding protein CYCLIC ADP-RIBOSE (cADPR), a nucleotide metabolite, mobilizes calcium from the intracellular stores through ryanodine receptors (RyRs). CD38, a membrane-bound glycoprotein, catalyzes the synthesis and degradation of cADPR. Studies from our laboratory and others have demonstrated that CD38/cADPRmediated calcium signaling and calcium release through RyR channels play a vital role in the regulation of calcium homeostasis in airway smooth muscle cells. Furthermore, the role of CD38/cADPR-mediated calcium signaling has been investigated in disease conditions such as asthma, diabetes, and pulmonary vasoconstriction. The review describes the evidence for the physiological and pathophysiological role of CD38/cADPR/RyR signaling in airway smooth muscle cells.

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Gamma-interferon modifies guinea pig airway functions in vitro

Cited by 20 publications

References 19 publications

Synthetic responses in airway smooth muscle

Synthetic responses in airway smooth muscle

RANTES (CCL5) Regulates Airway Responsiveness after Repeated Allergen Challenge

CD38/cyclic ADP-ribose signaling: role in the regulation of calcium homeostasis in airway smooth muscle

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