Increased MCP-1, RANTES, and MIP-1alpha in bronchoalveolar lavage fluid of allergic asthmatic patients.

Alam, Rafeul; York, Jennifer J.; Boyars, Michael; Stafford, Susan; Grant, J A; Lee, J; Forsythe, P.; Sim, Tommy C.; Ida, Nobuo

doi:10.1164/ajrccm.153.4.8616572

Cited by 284 publications

(179 citation statements)

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“…Chemokines present an important role in the physiopathology of asthma, such as activation of the inflammatory cascade, bronchial hyperresponsiveness, and airway remodeling (2,22,45,51). In accordance with current literature, our mouse model of allergic lung inflammation presented an increased expression of MCP-1 by inflammatory cells, both in the pulmonary arteries and lung parenchyma (Figs.…”

Section: Discussionsupporting

confidence: 89%

Aerobic conditioning and allergic pulmonary inflammation in mice. II. Effects on lung vascular and parenchymal inflammation and remodeling

Vieira¹,

Andrade²,

Duarte³

et al. 2008

American Journal of Physiology-Lung Cellular and Molecular Phys

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In addition, some studies demonstrated that aerobic training decreases chronic allergic inflammation in the airways; however, its effects on the pulmonary vessels and parenchyma have not been previously evaluated. Our objective was to test the hypothesis that aerobic conditioning reduces inflammation and remodeling in pulmonary vessels and parenchyma in a model of chronic allergic lung inflammation. Balb/c mice were sensitized at days 0, 14, 28, and 42 and challenged with ovalbumin (OVA) from day 21 to day 50. Aerobic training started on day 21 and continued until day 50. Pulmonary vessel and parenchyma inflammation and remodeling were evaluated by quantitative analysis of eosinophils and mononuclear cells and by collagen and elastin contents and smooth muscle thickness. Immunohistochemistry was performed to quantify the density of positive cells to interleukin (IL)-2, IL-4, IL-5, interferon-␥, IL-10, monocyte chemotatic protein (MCP)-1, nuclear factor (NF)-B p65, and insulin-like growth factor (IGF)-I. OVA exposure induced pulmonary blood vessels and parenchyma inflammation as well as increased expression of IL-4, IL-5, MCP-1, NF-B p65, and IGF-I by inflammatory cells were reduced by aerobic conditioning. OVA exposure also induced an increase in smooth muscle thickness and elastic and collagen contents in pulmonary vessels, which were reduced by aerobic conditioning. Aerobic conditioning increased the expression of IL-10 in sensitized mice. We conclude that aerobic conditioning decreases pulmonary vascular and parenchymal inflammation and remodeling in this experimental model of chronic allergic lung inflammation in mice.

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Section: Discussionsupporting

confidence: 89%

Aerobic conditioning and allergic pulmonary inflammation in mice. II. Effects on lung vascular and parenchymal inflammation and remodeling

Vieira¹,

Andrade²,

Duarte³

et al. 2008

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…This is consistent with data showing that its expression is upregulated in several inflammatory conditions, such as rheumatoid arthritis 17 and multiple sclerosis, 18 as well as asthma. [8][9][10][11] Our data indicated that −403 A is more common in asthmatics, both atopic and non-atopic. This observation is supported by Ying et al 19 who showed that RANTES expression was higher in bronchial mucosa from both types of asthma.…”

Section: Discussionmentioning

confidence: 99%

“…6,7 Furthermore, increased levels of RANTES and other members of the C-C family of chemokines (MIP-1␣, MCP-1) have been detected in the nasal secretions of atopic patients exposed to local allergen challenge 8 and were found in higher levels in the bronchial lavage fluid of patients with active asthma. 9 RANTES has also been found at significantly higher levels in patients during asthma attacks than in those with asymptomatic stages or in controls. 10 In addition, the number of eosinophils recruited to the lung is strongly correlated with the concentration of immunoreactive RANTES.…”

Section: Introductionmentioning

confidence: 95%

The −403 G→A promoter polymorphism in the RANTES gene is associated with atopy and asthma

et al. 2000

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Asthma is a complex inflammatory condition often associated with bronchial hyperreactivity and atopy. Genetic and environmental factors are implicated and several candidate genes have been implicated. Of these, the chemokine RANTES is responsible for the recruitment of inflammatory cells such as eosinophils and T-lymphocytes. We have recently identified a polymorphism within the RANTES promoter (−403 G →A) and have examined its role, using a PCR-RFLP assay, in the development of atopy and asthma in 201 Caucasian subjects. Atopic status was determined using skin prick testing and serum IgE levels. Severity of airway dysfunction was assessed using spirometric measurement (FEV 1 ) and methacholine challenge (PC 20 ). The −403 A allele was associated with an increased susceptibility to both atopy and asthma. Thus, the proportion of subjects carrying this allele was higher in each of atopic non-asthmatics, nonatopic asthmatics and atopic asthmatics compared with non-atopic, non-asthmatic controls. In particular, this allele was associated with skin test positivity but not IgE level. Homozygosity for the −403 A allele conferred a 6.5-fold increased risk of moderate/severe airway obstruction (FEV 1 р80% predicted), a marker for established asthma. Our data, whilst preliminary, indicate that the association of RANTES genotype with both atopy and asthma reflect independent effects, suggesting different mechanisms for the role of this chemokine in atopy and development of airway obstruction. Genes and Immunity (2000) 1, 509-514.

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“…It has been reported that CCL2 concentration in bronchoalveolar lavage fluid was found to be elevated in allergic asthmatic patients. 37 In addition, CCL2 can initiate leukocyte infiltration and inflammatory responses by inducing chemotaxis of monocytes, T lymphocytes, natural killer cells, eosinophils and basophils, and by degranulation and histamine release from both basophils and mast cells. [38][39][40] Taken together with the evidence demonstrating IL-33 as a chemoattractant for Th2 lymphocytes, 12 the significant CCL2 release from eosinophils upon IL-1b, IL-18 and IL-33 activation may facilitate the locomotion of both eosinophils and other leukocytes to promote the development of allergic inflammation.…”

Section: Il-33 Activates Eosinophilsmentioning

confidence: 99%

Intracellular signaling mechanisms regulating the activation of human eosinophils by the novel Th2 cytokine IL-33: implications for allergic inflammation

et al. 2009

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The novel interleukin (IL)-1 family cytokine IL-33 has been shown to activate T helper 2 (Th2) lymphocytes, mast cells and basophils to produce an array of proinflammatory cytokines, as well as to mediate blood eosinophilia, IgE secretion and hypertrophy of airway epithelium in mice. In the present study, we characterized the activation of human eosinophils by IL-33, and investigated the underlying intracellular signaling mechanisms. IL-33 markedly enhanced eosinophil survival and upregulated cell surface expression of the adhesion molecule intercellular adhesion molecule (ICAM)-1 on eosinophils, but it suppressed that of ICAM-3 and L-selectin. In addition, IL-33 mediates significant release of the proinflammatory cytokine IL-6 and the chemokines CXCL8 and CCL2. We found that IL-33-mediated enhancement of survival, induction of adhesion molecules, and release of cytokines and chemokines were differentially regulated by activation of the nuclear factor (NF)-kB, p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase (ERK) pathways. Furthermore, we compared the above IL-33 activities with two structurally and functionally related cytokines, IL-1b and IL-18. IL-1b, but not IL-18, markedly upregulated cell surface expression of ICAM-1. IL-1b and IL-18 also significantly enhanced eosinophil survival, and induced the release of IL-6 and chemokines CXCL8 and CCL2 via the activation of the NF-kB, p38 MAPK and ERK pathways. Synergistic effects on the release of IL-6 were also observed in combined treatment with IL-1b, IL-18 and IL-33. Taken together, our findings provide insight into IL-33-mediated activation of eosinophils via differential intracellular signaling cascades in the immunopathogenesis of allergic inflammation.

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Increased MCP-1, RANTES, and MIP-1alpha in bronchoalveolar lavage fluid of allergic asthmatic patients.

Cited by 284 publications

References 0 publications

Aerobic conditioning and allergic pulmonary inflammation in mice. II. Effects on lung vascular and parenchymal inflammation and remodeling

Aerobic conditioning and allergic pulmonary inflammation in mice. II. Effects on lung vascular and parenchymal inflammation and remodeling

The −403 G→A promoter polymorphism in the RANTES gene is associated with atopy and asthma

Intracellular signaling mechanisms regulating the activation of human eosinophils by the novel Th2 cytokine IL-33: implications for allergic inflammation

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