Effects of Reactive Oxygen and Nitrogen Metabolites on RANTES. and IL-5-Induced Eosinophil Chemotactic Activity in vitro

Sato, Etsuro; Simpson, Keith L.; Grisham, Matthew B.; Koyama, Sekiya; Robbins, Richard

doi:10.1016/s0002-9440(10)65154-1

Cited by 39 publications

(29 citation statements)

References 51 publications

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“…This corroborates a previous study demonstrating that incubation of human eosinophils with peroxynitrite did not affect the eotaxin-induced cell chemotaxis [152]. However, in this same study, incubation of eotaxin (0.5-500 ng/ml) with peroxynitrite (1-1000 µM) for 2 h prior to the chemotaxis assays resulted in a marked reduction in the eosinophil chemotaxis, an effect prevented by addition of L-tyrosine to eotaxin before incubating with peroxynitrite [122,152]. Enzyme-linked immunosorbent assay (ELISA) further revealed that peroxynitrite resulted in 3-NT formation on eotaxin, which is accompanied by a reduction of eotaxin binding to eosinophils [152].…”

Section: Role Of Peroxynitrite In the No-mediated Inflammatory Actionssupporting

confidence: 92%

“…In addition to changes in adhesion molecule function, NO may also modulate cytoskeletal rearrangements, cytokine production by the endothelium and reduce oxidative stress [107,115,119,122,123], all of which play an important role in leukocyte-endothelium adhesive interactions. In summary, overwhelming evidence indicates that nitric oxide has an important role in inhibiting leukocyte-endothelium and leukocyte-ECM interactions by limiting the expression and functional activity of the adhesion molecules expressed by both the leukocyte and by the endothelial cells, whether this actually results in alterations in leukocyte migration into inflammatory sites is unclear, as yet, since the conflicting evidence for the role of NO in leukocyte migration is unclear and may depend upon a number of factors such as cell type and quantity of NO available.…”

Section: In Vitro Evidence For a Role Of No In Leukocyte Adhesive Intmentioning

confidence: 99%

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Modulation of Eosinophil Functions by Nitric Oxide: Cyclic GMPdependent and -independent Mechanisms

Ferreira¹,

Conran²,

Antunes³

2006

AIAAMC

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Recruitment of eosinophils into tissues is a feature of a variety of allergic diseases, including asthma and nasal allergy. Eosinophils secrete several preformed granule proteins (eosinophil peroxidase, major basic protein, eosinophil cationic protein and eosinophil-derived neurotoxin) and newly-generated substances (oxygen-derived toxic metabolites, lipid mediators, cytokines and chemokines), which may contribute to the exacerbation of the allergic diseases. In the past decade, NO has been recognized as a major immunomodulatory mediator of inflammatory responses, particularly in the lung, where it is believed to play a pivotal role in modulating pulmonary eosinophilia and airways hyperresponsiveness in both allergic animals and humans, as evidenced by functional, biochemical and immunohistochemical studies. The NOcGMP signaling cascade was initially implicated in the modulation of eosinophil functions; however, additional studies have demonstrated that direct cGMP-independent mechanisms may also play important roles in eosinophil functions. Much progress in understanding the influence of NO on eosinophil functions has been achieved with the use of selective and non-selective NOS inhibitors, as well as NO-donor compounds, along with NOS isoform gene knock-out mice. However, these studies have resulted in numerous controversies and conflicting findings, possibly as a consequence of the diversity of experimental models used, animal species employed, methods of immunization and challenge with allergens, amongst others. The present review summarizes the role of NO in modulating, in vivo and in vitro, eosinophil adhesion, chemotaxis, airways hyperresponsiveness and apoptosis, outlining the conflicting findings in the literature, with emphasis on the allergic inflammatory responses.

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Section: Role Of Peroxynitrite In the No-mediated Inflammatory Actionssupporting

confidence: 92%

Section: In Vitro Evidence For a Role Of No In Leukocyte Adhesive Intmentioning

confidence: 99%

Modulation of Eosinophil Functions by Nitric Oxide: Cyclic GMPdependent and -independent Mechanisms

Ferreira¹,

Conran²,

Antunes³

2006

AIAAMC

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“…RANTES has also been shown to enhance the production of IgE and IgG4 by activated B cells [7]. In addition, RANTES recruits eosinophils and T cells into the airways during asthma [8] and allergic airway disease [9] and it may contribute to their immunopathology [10]. Eosinophils cause tissue damage and promote allergic disease in the lung through the release of toxic proteases, lipid mediators, cytokines, and oxygen free radicals [11], whereas T cells are a source of proallergic cytokines, including IL-4 and IL-13 [12].…”

Section: Introductionmentioning

confidence: 99%

RANTES Gene Promoter Polymorphisms Are Associated with Bronchial Hyperresponsiveness in Korean Children with Asthma

Sohn

Kim

et al. 2007

Lung

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Regulated upon activation in normal T cells, expressed, and secreted (RANTES) protein is abundantly expressed during atopic asthma, suggesting that it is an important mediator of this disease. The aim of this study was to evaluate the possible role of RANTES promoter polymorphisms in children with asthma. We genotyped 271 children with atopic asthma, 55 children with nonatopic asthma, and 253 control children for allelic determinants at two polymorphic sites in the promoter region at positions -403G[A and -28C[G by restriction fragment length polymorphism methods. There was no significant difference in genotype and allele frequencies of the RANTES -403G[A and -28C[G polymorphisms when the atopic asthma, nonatopic asthma, and control groups were compared. However, atopic asthmatic patients who were homozygous GG for the RANTES -28C[G tended to have lower PC 20 methacholine than those carrying the wild genotype. In addition, a significantly lower PC 20 was demonstrated for the homozygous haplotype -403A/-28G in asthmatic children. The polymorphisms within the RANTES promoter may have a disease-modifying effect in Korean children with asthma.

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“…The implications of nitration for chemokine function are divers. For CCL5, nitration was shown to significantly impair the potency of the chemokine to chemoattract eosinophils in vitro (162). Concerning CCL2, conflicting results have been reported.…”

Section: Chemokinesmentioning

confidence: 99%

Regulation of Chemokine Activity – A Focus on the Role of Dipeptidyl Peptidase IV/CD26

et al. 2016

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Chemokines are small, chemotactic proteins that play a crucial role in leukocyte migration and are, therefore, essential for proper functioning of the immune system. Chemokines exert their chemotactic effect by activation of chemokine receptors, which are G protein-coupled receptors (GPCRs), and interaction with glycosaminoglycans (GAGs). Furthermore, the exact chemokine function is modulated at the level of posttranslational modifications. Among the different types of posttranslational modifications that were found to occur in vitro and in vivo, i.e., proteolysis, citrullination, glycosylation, and nitration, NH2-terminal proteolysis of chemokines has been described most intensively. Since the NH2-terminal chemokine domain mediates receptor interaction, NH2-terminal modification by limited proteolysis or amino acid side chain modification can drastically affect their biological activity. An enzyme that has been shown to provoke NH2-terminal proteolysis of various chemokines is dipeptidyl peptidase IV or CD26. This multifunctional protein is a serine protease that preferably cleaves dipeptides from the NH2-terminal region of peptides and proteins with a proline or alanine residue in the penultimate position. Various chemokines possess such a proline or alanine residue, and CD26-truncated forms of these chemokines have been identified in cell culture supernatant as well as in body fluids. The effects of CD26-mediated proteolysis in the context of chemokines turned out to be highly complex. Depending on the chemokine ligand, loss of these two NH2-terminal amino acids can result in either an increased or a decreased biological activity, enhanced receptor specificity, inactivation of the chemokine ligand, or generation of receptor antagonists. Since chemokines direct leukocyte migration in homeostatic as well as pathophysiologic conditions, CD26-mediated proteolytic processing of these chemotactic proteins may have significant consequences for appropriate functioning of the immune system. After introducing the chemokine family together with the GPCRs and GAGs, as main interaction partners of chemokines, and discussing the different forms of posttranslational modifications, this review will focus on the intriguing relationship of chemokines with the serine protease CD26.

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Effects of Reactive Oxygen and Nitrogen Metabolites on RANTES. and IL-5-Induced Eosinophil Chemotactic Activity in vitro

Cited by 39 publications

References 51 publications

Modulation of Eosinophil Functions by Nitric Oxide: Cyclic GMPdependent and -independent Mechanisms

Modulation of Eosinophil Functions by Nitric Oxide: Cyclic GMPdependent and -independent Mechanisms

RANTES Gene Promoter Polymorphisms Are Associated with Bronchial Hyperresponsiveness in Korean Children with Asthma

Regulation of Chemokine Activity – A Focus on the Role of Dipeptidyl Peptidase IV/CD26

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