Glucocorticoid-induced surface expression of annexin 1 blocks β2-integrin adhesion of human eosinophils to intercellular adhesion molecule 1 surrogate protein

Liu, Jie; Zhu, Xiangdong; Myo, Saori; Lambertino, Anissa; Xu, Chang; Boetticher, Evan; Muñoz, N. M.; Sano, Masaaki; Cordoba, Martha; Learoyd, Jonathan; Meliton, Angelo Y.; Johnson, Malcolm; Leff, Alan R.

doi:10.1016/j.jaci.2004.11.010

Cited by 18 publications

(26 citation statements)

References 23 publications

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“…AnxA1 was first identified as a factor that was released from GC-stimulated cells in vitro or in vivo, and exerted anti-inflammatory effects mirroring those of GCs. Most notably it inhibited release of proinflammatory prostaglandins, and impaired leukocyte extravasation at sites of inflammation (Chatterjee et al, 2005;de Coupade et al, 2003;Gavins et al, 2003;Lim and Pervaiz, 2007;Liu et al, 2005;Parente and Solito, 2004). AnxA1 is relocalized from the cytoplasm to the plasma membrane in response to a variety of agonists including GCs, and can be externalized or secreted via an uncharacterized mechanism.…”

Section: Annexin A1mentioning

confidence: 99%

Anti-inflammatory functions of glucocorticoid-induced genes

Clark

2007

Molecular and Cellular Endocrinology

238

193

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Section: Annexin A1mentioning

confidence: 99%

Anti-inflammatory functions of glucocorticoid-induced genes

Clark

2007

Molecular and Cellular Endocrinology

238

193

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“…Prior in vivo and in vitro studies have demonstrated that blockade of gIVaPLA 2 inhibits 1) cellular adhesion/migration of eosinophils and lymphocytes (12)(13)(14), 2) synthesis of arachidonate metabolites (15)(16)(17)(18)(19)(20), and 3) airway narrowing (21)(22)(23). Mammalian secretory 14-kDa PLA 2 s, e, g., gVPLA 2, gIIaPLA 2 , and gXPLA 2 , are inflammatory enzymes that are involved directly and indirectly in inducing inflammatory and allergic processes; however, the mode of action of these sPLA 2 isoforms has not been fully established.…”

mentioning

confidence: 99%

“…Other studies have demonstrated substantially greater AHR in immunosensitized gIVaPLA 2 wild-type (WT) mice than in gIVaPLA 2 knockout mice (23,34,37). Although much attention has been focused on gIVaPLA 2 as the critical regulating enzyme in integrin adhesion (12)(13)(14) and eicosanoid generation (15)(16)(17)(18)(19)(20), the signal initiating stimulus that triggers the activation of inflammatory cells to cause cell migration and AHR in chronic asthma has not been defined. We have demonstrated that gVPLA 2 can trigger the biosynthesis and release of LTB 4 from human neutrophils (32,33) in a gIVaPLA 2 -dependent manner and LTC 4 from human eosinophils in a gIVaPLA 2 -independent manner (34,35).…”

mentioning

confidence: 99%

Deletion of Secretory Group V Phospholipase A2 Attenuates Cell Migration and Airway Hyperresponsiveness in Immunosensitized Mice

Muñoz

Meliton

Jonathan

et al. 2007

The Journal of Immunology

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We investigated the role of group V phospholipase A2 (gVPLA2) in OVA-induced inflammatory cell migration and airway hyperresponsiveness (AHR) in C57BL/6 mice. Repeated allergen challenge induced biosynthesis of gVPLA2 in airways. By aerosol, gVPLA2 caused dose-related increase in airway resistance in saline-treated mice; in allergic mice, gVPLA2 caused persistent airway narrowing. Neither group IIa phospholipase A2, a close homolog of gVPLA2, nor W31A, an inactive gVPLA2 mutant with reduced activity, caused airway narrowing in immune-sensitized mice. Pretreatment with MCL-3G1, a blocking Ab against gVPLA2, before OVA challenge blocked fully gVPLA2-induced cell migration and airway narrowing as marked by reduction of migrating leukocytes in bronchoalveolar lavage fluid and decreased airway resistance. We also assessed whether nonspecific AHR caused by methacholine challenge was elicited by gVPLA2 secreted from resident airway cells of immune-sensitized mice. MCL-3G1 also blocked methacholine-induced airway bronchoconstriction in allergic mice. Blockade of bronchoconstriction by MCL-3G1 was replicated in allergic pla2g5−/− mice, which lack the gene encoding gVPLA2. Bronchoconstriction caused by gVPLA2 in pla2g4−/− mice was comparable to that in pla2g4+/+ mice. Our data demonstrate that gVPLA2 is a critical messenger enzyme in the development of AHR and regulation of cell migration during immunosensitization by a pathway that is independent of group IVa phospholipase A2.

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“…ALDH1A1 can perturb murine hematopoiesis by promoting myeloid differentiation at the expense of lymphopoiesis [29]. Glucocorticoid-induced surface expression of ANXA1 blocks beta 2-integrin adhesion of human eosinophils to intercellular adhesion molecule 1 surrogate protein [15]. IL33 potently induces effector functions and cytokine production, enhances adhesion, and prolongs survival of eosinophils [4,5,26,36].…”

Section: Discussionmentioning

confidence: 99%

Genes for Difference in Eosinophilic Phenotype between MES and BN.MES-Cybames Rats Are on Chromosomes 9, 5, and 1

et al. 2011

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Abstract:The Matsumoto Eosinophilia Shinshu (MES) rat strain develops hereditary blood eosinophilia due to the mutant Cyba mes gene. In contrast, BN.MES-Cyba mes congenic rats, in which the mutant Cyba mes gene introduced into the background of the BN strain, have a normal blood eosinophil level despite showing robust proliferation of eosinophils in the bone marrow. However, the congenic rats manifest focal necrosis with eosinophilic infiltration in the liver, a phenotype rarely observed in the original MES rat strain. To elucidate the genetic basis for the strain differences, (MES × BN.MES-Cyba mes )F 2 rats were bred, and genetic analyses of phenotypes for eosinophilia were performed. Blood and bone marrow eosinophil levels in the F 2 rats showed broad distributions, suggesting that the traits were under the influence of multiple genes. Genetic association studies revealed that BN-derived marker loci on chromosomes 9 and 5 were responsible for the increase in eosinophil level in the bone marrow, decrease in blood eosinophil level, and the induction of focal necrosis with eosinophilic infiltration in the liver. The BN-derived allele of the marker gene on chromosome 1 was responsible for the decrease of both bone marrow and blood eosinophil levels. These data suggest the existence of genes characterizing/distinguishing the eosinophilic phenotypes of MES and BN.MES-Cyba mes on these chromosomes, and form the basis for positional cloning studies of the genes. These studies will advance the understanding of the mechanisms involved in eosinophil mobilization from the bone marrow and recruitment to the organs.

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Glucocorticoid-induced surface expression of annexin 1 blocks β2-integrin adhesion of human eosinophils to intercellular adhesion molecule 1 surrogate protein

Cited by 18 publications

References 23 publications

Anti-inflammatory functions of glucocorticoid-induced genes

Anti-inflammatory functions of glucocorticoid-induced genes

Deletion of Secretory Group V Phospholipase A2 Attenuates Cell Migration and Airway Hyperresponsiveness in Immunosensitized Mice

Genes for Difference in Eosinophilic Phenotype between MES and BN.MES-Cybames Rats Are on Chromosomes 9, 5, and 1

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