Differential serum protein markers and the clinical severity of asthma

Meyer, Norbert; Nuss, Sarah; Rothe, Thomás; Siebenhüner, Alexander; Akdiş, Cezmi A.; Menz, Günter

doi:10.2147/jaa.s53920

Cited by 20 publications

(15 citation statements)

References 26 publications

(31 reference statements)

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“…In support of this, CCL27 concentrations in the blood are correlated as well to various markers of T H 2 response (Eotaxin‐1) and/or severe asthma (YKL‐40) . Together with previous reports documenting that CCL27 blood levels are higher in patients with either poorly controlled asthma, psoriasis, or atopic dermatitis, this suggests that this chemokine is upregulated in association with various chronic inflammatory conditions.…”

Section: Discussionsupporting

confidence: 80%

“…In this cohort of 62 subjects, CCL27 plasma concentrations also correlated with levels of several markers associated with asthma severity, including eotaxin‐1 ( P = 0.045), MCP‐1 ( P = 0.0067), osteopontin ( P = 0.016), and YKL‐40 ( P = 0.0024) (Figure C). Noteworthy, we did not observe significant correlations between CCL27 concentration and periostin or ECP concentrations (data not shown, ie, two other known asthma‐related markers). Altogether, both CCR10 + ILC2 frequencies and CCL27 concentrations in the blood reflect asthma severity.…”

Section: Resultsmentioning

confidence: 69%

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CCR10⁺ILC2s with ILC1‐like properties exhibit a protective function in severe allergic asthma

Beuraud

Lombardi

Luce

et al. 2018

Allergy

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Background:We previously showed that patients with severe allergic asthma have high numbers of circulating ILC2s expressing CCR10. Method:Herein, CCR10 + ILC2s were further analyzed in the blood of healthy individuals or patients with allergic and non−allergic asthma. Characteristics of human CCR10 + and CCR10 − ILC2s were assessed by flow cytometry as well as single-cell multiplex RT-qPCR. The role of CCR10 + ILC2s in asthma pathophysiology was studied in allergen-treated mice.Results: When compared to healthy controls, CCR10 + ILC2s are enriched in the blood of both allergic and non-allergic severe asthmatic patients, and these cells are recruited to the lungs. Plasma concentrations of the CCR10 ligand CCL27 are significantly increased in severe asthmatics when compared to non-asthmatic patients.CCR10 + ILC2s secrete little T H 2 cytokines, but exhibit ILC1-like properties, including a capacity to produce IFN-γ. Also, single-cell analysis reveals that the CCR10 + ILC2 subset is enriched in cells expressing amphiregulin. CCR10 + ILC2 depletion, as well as blocking of IFN-γ activity, exacerbates airway hyperreactivity in allergen-challenged mice, providing evidence for a protective role of these cells in allergic inflammation. Conclusions:Frequencies of circulating CCR10 + ILC2s and CCL27 plasma concentrations represent candidate markers of asthma severity. The characterization of CCR10 + ILC2s in human samples and in mouse asthma models suggests that these cells downregulate allergic inflammation through IFN-γ production.

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Section: Discussionsupporting

confidence: 80%

Section: Resultsmentioning

confidence: 69%

CCR10⁺ILC2s with ILC1‐like properties exhibit a protective function in severe allergic asthma

Beuraud

Lombardi

Luce

et al. 2018

Allergy

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“…2013; 4 Meyer et al . 2014 and are representative of asthmatic human values (normal values are given for comparisons). Lysophosphatidic acid concentrations are taken from 5 Jendzjowsky et al .…”

Section: Resultsmentioning

confidence: 99%

“…Given that we used concentrations of asthma-associated Th2 cytokines reported in asthmatic plasma (Lilly et al 1999;Kokkonen et al 2010;Kleiner et al 2013;Meyer et al 2014;Akiki et al 2017) (Table 1), and the carotid bodies produce bronchoconstriction (Nadel & Widdicombe, 1962;Iscoe & Fisher, 1995;Mazzone & Canning, 2002;Habre et al 2010;Jendzjowsky et al 2018), we suggest that multiple asthmakines are capable of activating the PKCε-TRPV1 pathway, and -in different circumstances or disease states -different combinations may trigger the carotid body bronchoconstriction reflex.…”

Section: The Role Of the Carotid Body Pkcε-trpv1 Pathway In Asthmamentioning

confidence: 99%

PKCε stimulation of TRPV1 orchestrates carotid body responses to asthmakines

Jendzjowsky

Roy

Iftinca

et al. 2020

The Journal of Physiology

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We have previously shown that carotid body stimulation by lysophosphatidic acid elicits a reflex stimulation of vagal efferent activity sufficient to cause bronchoconstriction in asthmatic rats. r Here, we show that pathophysiological concentrations of asthma-associated prototypical Th2 cytokines also stimulate the carotid bodies. r Stimulation of the carotid bodies by these asthmakines involves a PKCε-transient receptor potential vanilloid 1 (TRPV1) signalling mechanism likely dependent on TRPV1 S502 and T704 phosphorylation sites. r As the carotid bodies' oxygen sensitivity is independent of PKCε-TRPV1 signalling, systemic blockade of PKCε may provide a novel therapeutic target to reduce allergen-induced asthmatic bronchoconstriction. r Consistent with the therapeutic potential of blocking the PKCε-TRPV1 pathway, systemic delivery of a PKCε-blocking peptide suppresses asthmatic respiratory distress in response to allergen and reduces airway hyperresponsiveness to bradykinin.

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“…An eosinophil-dominant inflammation was reported in six studies. Treatment optimisation was found to improve FEV 1 in three studies 23 39 40…”

Section: Cluster Analysis: Asthma–copd Overlap As An Airway Disease Pmentioning

confidence: 99%

Asthma-COPD overlap 2015: now we are six

Gibson

McDonald

2015

Thorax

184

156

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BackgroundThe overlap between asthma and COPD is increasingly recognised. This review examines the new insights, treatment and remaining knowledge gaps for asthma–COPD overlap.MethodA systematic literature review of cluster analyses of asthma and COPD was performed. Articles from 2009 to the present dealing with prevalence, morbidity and treatment of asthma–COPD overlap were identified and reviewed.ResultsAsthma–COPD overlap was consistently recognised in studies using a variety of different study designs and sampling. The prevalence was approximately 20% in patients with obstructive airways diseases. Asthma–COPD overlap was associated with increased morbidity and possibly an increased mortality and comorbidity. There was evidence of a heterogeneous pattern of airway inflammation that included eosinophilic (in adult asthma), neutrophilic or mixed patterns (in severe asthma and COPD). Systemic inflammation was present in asthma–COPD overlap and resembled that of COPD. Within asthma–COPD overlap, there is evidence of different subgroups, and recognition using bronchodilator responsiveness has not been successful. Guidelines generally recommend a serial approach to assessment, with treatment recommendations dominated by an asthma paradigm. Research is needed into key clinical features that impact outcome, mechanisms and treatment approaches in asthma–COPD overlap. Identifying and treating disease components by multidimensional assessment shows promise.ConclusionsAsthma–COPD overlap has drawn attention to the significant heterogeneity that exists within obstructive airway diseases. It should be replaced by novel approaches that identify and manage the components of this heterogeneity, such as multidimensional assessment and treatment. Future research is needed to test these novel and personalised approaches.

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Differential serum protein markers and the clinical severity of asthma

Cited by 20 publications

References 26 publications

CCR10⁺ILC2s with ILC1‐like properties exhibit a protective function in severe allergic asthma

CCR10⁺ILC2s with ILC1‐like properties exhibit a protective function in severe allergic asthma

PKCε stimulation of TRPV1 orchestrates carotid body responses to asthmakines

Asthma-COPD overlap 2015: now we are six

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Differential serum protein markers and the clinical severity of asthma

Cited by 20 publications

References 26 publications

CCR10+ILC2s with ILC1‐like properties exhibit a protective function in severe allergic asthma

CCR10+ILC2s with ILC1‐like properties exhibit a protective function in severe allergic asthma

PKCε stimulation of TRPV1 orchestrates carotid body responses to asthmakines

Asthma-COPD overlap 2015: now we are six

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CCR10⁺ILC2s with ILC1‐like properties exhibit a protective function in severe allergic asthma

CCR10⁺ILC2s with ILC1‐like properties exhibit a protective function in severe allergic asthma