Airway cytokine expression measured by means of protein array in exhaled breath condensate: Correlation with physiologic properties in asthmatic patients

Matsunaga, Kazuto; Yanagisawa, Satoru; Ichikawa, Tomohiro; Ueshima, Kazuhito; Akamatsu, Keiichiro; Hirano, Tsunahiko; Nakanishi, Masayoshi; Yamagata, Toshiyuki; Minakata, Yoshiaki; Ichinose, Masakazu

doi:10.1016/j.jaci.2006.04.020

Cited by 107 publications

(111 citation statements)

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“…Exhaled breath condensate MATSUNAGA et al [42] published a study on the concentrations of IL-17A protein in exhaled breath condensate from patients with asthma and healthy control subjects. The subjects were nonsmokers and who were not receiving any glucocorticoid treatment.…”

Section: Sputum Samplesmentioning

confidence: 99%

“…In accordance with most of the studies on BAL and sputum samples, the results of this study suggest that IL-17A protein is moderately increased in patients with mild asthma, compared with healthy control subjects. It is of particular mechanistic interest that MATSUNAGA et al [42] obtained indications that the increase in IL-17A among these patients with asthma is associated with a corresponding increase in IL-8, tumour necrosis factor (TNF)-a and transforming growth factor (TGF)-b; cytokines that are associated with the mobilisation of neutrophils and Th17 cells [7][8][9][10][11][12][13]. It is also of mechanistic interest that MATSUNAGA et al [42] detected a trend towards a correlation between the concentration of ''exhaled'' IL-17A and airway obstruction in patients with asthma.…”

Section: Sputum Samplesmentioning

confidence: 99%

“…It is also of mechanistic interest that MATSUNAGA et al [42] detected a trend towards a correlation between the concentration of ''exhaled'' IL-17A and airway obstruction in patients with asthma. Unfortunately, the utilised technique did not allow the investigators to relate exhaled IL-17A to the accumulation of luminal neutrophils [42].…”

Section: Sputum Samplesmentioning

confidence: 99%

“…It remains to be evaluated whether Th17 or Tc17 cells in the airways of patients with asthma share characteristics with the corresponding blood cells [12,13,48,[51][52][53][54][55][56][57]. Moreover, the documentation of expression for IL-17A in invariant natural killer T-cells and in mucosal-associated invariant T-cells from human subjects is intriguing but further study is needed given that there are no published studies addressing these cell types in the airways of patients with asthma [11,13,42,44,48,[50][51][52][53][54][55][56][57][58][59][60][61][62][63][64][65][66].…”

Section: Multiple Cellular Sourcesmentioning

confidence: 99%

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Interleukin-17 cytokine signalling in patients with asthma

Lindén

Dahlén

2014

Eur Respir J

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Asthma remains a global health problem and, therefore, more effective pharmacotherapy is needed. This is particularly true for chronic and severe asthma. In these clinical phenotypes, chronic inflammation involving neutrophils is likely to play a pathogenic role, making it interesting to target cytokine signalling involved in the accumulation of neutrophils. Therefore, it is of interest that the archetype T-helper 17 cell cytokine interleukin (IL)-17A, perhaps also IL-17F, controls neutrophil accumulation, mucus secretion, macrophage mobilisation and smooth muscle reactivity in various experimental airway models. However, much less is known about the involvement of signalling via IL-17 cytokines in humans with asthma. Existing evidence suggests that these cytokines are released from several types of immune cells in asthma and, for IL-17A, there is a local increase associated with disease severity, with the mobilisation of neutrophils and smooth muscle cells locally in the airways. Even though the causative role of IL-17 cytokines remains unclear, there is potential for clinical utility in targeting IL-17A specifically in patients with moderate-to-severe asthma and high reversibility. There is a need for new and well-powered clinical investigations of signalling via IL-17 cytokines in this clinical phenotype. @ERSpublications There is potential utility for drugs targeting IL-17 cytokine signalling in a sub-group of patients with asthma

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Section: Sputum Samplesmentioning

confidence: 99%

Section: Sputum Samplesmentioning

confidence: 99%

Section: Sputum Samplesmentioning

confidence: 99%

Section: Multiple Cellular Sourcesmentioning

confidence: 99%

See 2 more Smart Citations

Interleukin-17 cytokine signalling in patients with asthma

Lindén

Dahlén

2014

Eur Respir J

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“…TNF␣, either newly synthesized or preformed and stored constitutively within the mast cell granules, is coreleased with other potent mediators such as histamine and tryptase via the IgE-dependent mechanism (9, 21, 47). TNF␣ was detected in bronchoalveolar lavage fluid, sputum, exhaled breath condensate, and serum of asthmatic patients during asthmatic attack or following antigen inhalation challenge (12,33,39). Furthermore, it has been shown that TNF␣ is released from sensitized human and mouse lung tissue in response to antigen challenge (21,33,47).…”

mentioning

confidence: 99%

Calcium transient evoked by TRPV1 activators is enhanced by tumor necrosis factor-α in rat pulmonary sensory neurons

Gu²,

Lin³

et al. 2010

American Journal of Physiology-Lung Cellular and Molecular Phys

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Hu Y, Gu Q, Lin RL, Kryscio R, Lee LY. Calcium transient evoked by TRPV1 activators is enhanced by tumor necrosis factor-␣ in rat pulmonary sensory neurons. Am J Physiol Lung Cell Mol Physiol 299: L483-L492, 2010. First published July 16, 2010 doi:10.1152/ajplung.00111.2010.-TNF␣, a proinflammatory cytokine known to be involved in the pathogenesis of allergic asthma, has been shown to induce hyperalgesia in somatic tissue via a sensitizing effect on dorsal root ganglion neurons expressing transient receptor potential vanilloid type 1 receptor (TRPV1). Because TRPV1-expressing pulmonary sensory neurons play an important role in regulating airway function, this study was carried out to determine whether TNF␣ alters the sensitivity of these neurons to chemical activators. Responses of isolated nodose and jugular ganglion neurons innervating the rat lungs were determined by measuring the transient increase in intracellular Ca 2ϩ concentration ([Ca 2ϩ ]i). Our results showed the following. 1) A pretreatment with TNF␣ (50 ng/ml) for ϳ24 h increased significantly the peak ⌬[Ca 2ϩ ]i evoked by capsaicin (Cap) in these neurons. A pretreatment with the same concentration of TNF␣ for a longer duration (ϳ48 h) did not further increase the response, but pretreatment for a shorter duration (1 h) or with a lower concentration (25 ng/ml, 24 h) failed to enhance the Cap sensitivity.2) The same TNF␣ pretreatment also induced similar but less pronounced and less uniform increases in the responses to acid (pH 6.5-5.5), 2-aminoethoxydiphenyl borate (2-APB), a common activator of TRPV1, V2, and V3 channels, and allyl isothiocyanate (AITC), a selective activator of TRPA1 channel. 3) In sharp contrast, the responses to ATP, ACh, and KCl were not affected by TNF␣. 4) The TNF␣-induced hypersensitivity to Cap was not prevented by pretreatment with indomethacin (30 M). 5) The immunoreactivity to both TNF receptor types 1 and 2 were detected in rat vagal pulmonary sensory neurons. In conclusion, prolonged treatment with TNF␣ induces a pronounced potentiating effect on the responses of isolated pulmonary sensory neurons to TRPV1 activators. This action of TNF␣ may contribute in part to the airway hyperresponsiveness induced by this cytokine. intracellular calcium; pulmonary afferent; transient receptor potential vanilloid type 1; airway inflammation; asthma AN IMPORTANT ROLE OF TNF␣ in the pathogenesis of allergic asthma has been extensively documented (6,9,28,47). TNF␣ can be released from a variety of cell types in the airways, particularly macrophages, monocytes, and mast cells. TNF␣, either newly synthesized or preformed and stored constitutively within the mast cell granules, is coreleased with other potent mediators such as histamine and tryptase via the IgE-dependent mechanism (9, 21, 47). TNF␣ was detected in bronchoalveolar lavage fluid, sputum, exhaled breath condensate, and serum of asthmatic patients during asthmatic attack or following antigen inhalation challenge (12,33,39). Furthermore, it has been shown that TNF␣ is releas...

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