Fibrocyte trafficking in patients with chronic obstructive asthma and during an acute asthma exacerbation

Wang, Chun Hua; Punde, T. H.; Huang, Chih-Fang; Chou, Pai Chien; Huang, Tzu Ting; Wu, Wen‐guey; Liu, Cheng-Hsien; Chung, Kian Fan; Kuo, Han Pin

doi:10.1016/j.jaci.2014.09.011

Cited by 44 publications

(68 citation statements)

References 29 publications

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“…In the peripheral blood, CD45 severe asthma (182). CXCR4 and CCR7 mediated fibrocyte transmigration in acute asthma exacerbation and in chronic obstructive asthma, respectively (183). Due to the systemic involvement, asthma exacerbation can also be monitored or even predicted by urinary metabolites including arachidonic derivatives such as leukotrienes (184,185) and urinary trypsin inhibitor (186).…”

Section: Biomarkers For Disease Severity and Exacerbationmentioning

confidence: 99%

Current and future biomarkers in allergic asthma

Zissler

Bieren

Jakwerth

et al. 2016

Allergy

107

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Diagnosis early in life, sensitization, asthma endotypes, monitoring of disease and treatment progression are key motivations for the exploration of biomarkers for allergic rhinitis and allergic asthma. The number of genes related to allergic rhinitis and allergic asthma increases steadily; however, prognostic genes have not yet entered clinical application. We hypothesize that the combination of multiple genes may generate biomarkers with prognostic potential. The current review attempts to group more than 161 different potential biomarkers involved in respiratory inflammation to pave the way for future classifiers. The potential biomarkers are categorized into either epithelial or infiltrate-derived or mixed origin, epithelial biomarkers. Furthermore, surface markers were grouped into cell-typespecific categories. The current literature provides multiple biomarkers for potential asthma endotypes that are related to T-cell phenotypes such as Th1, Th2, Th9, Th17, Th22 and Tregs and their lead cytokines. Eosinophilic and neutrophilic asthma endotypes are also classified by epithelium-derived CCL-26 and osteopontin, respectively. There are currently about 20 epithelium-derived biomarkers exclusively derived from epithelium, which are likely to innovate biomarker panels as they are easy to sample. This article systematically reviews and categorizes genes and collects current evidence that may promote these biomarkers to become part of allergic rhinitis or allergic asthma classifiers with high prognostic value.

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Section: Biomarkers For Disease Severity and Exacerbationmentioning

confidence: 99%

Current and future biomarkers in allergic asthma

Zissler

Bieren

Jakwerth

et al. 2016

Allergy

107

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“…All the available studies consistently indicate that the numbers of circulating Fcs are very low in normal subjects (Table 1) and that these cells are rarely detected in the bronchial mucosa of healthy individuals (Nihlberg et al, 2006;Saunders et al, 2009;Wang et al, 2015) or in their induced sputum (Bellini et al, 2012) and bronchoalveolar lavage (Nihlberg et al, 2006). In asthmatic patients, the numbers of circulating Fcs are in the normal range values when their disease, irrespective of its severity, is adequately controlled by the treatment they are receiving (Saunders et al, 2009;Bianchetti et al, 2012a; (Table 1).…”

Section: Prognostic Roles In Asthmamentioning

confidence: 90%

“…Moreover, the sputum fluid phase from patients with treatment-resistant severe asthma, but not that from patients with adequately-controlled disease, has a strong chemotactic effect on autologous circulating Fcs, and over 50% of this chemotactic activity is attributable to the combined presence of high amounts of CCL5, CCL11, and CCL24 (Isgrò et al, 2013b). Since Fcs express CCR7 (Abe et al, 2001), the CCR7 ligands CCL19 and CCL21 (also known as secondary lymphoid cytokine) may potentially contribute to the airway recruitment of these cells, albeit only to a small extent, as suggested by blocking experiments in an animal model of chronic allergic asthma with induced airway remodeling (Mattoli, 2006) and in vitro experiments with Fcs from asthmatic patients (Wang et al, 2015). Epithelial cellderived endothelin-1 (ET-1) contributes to the expansion of the population of recruited Fcs in concert with IL-33 (Schmidt et al, 2003;Bianchetti et al, 2012a;Bellini et al, 2013) (Fig.…”

Section: Factors Regulating Fc Trafficking and Activationmentioning

confidence: 99%

“…In asthmatic patients, the numbers of circulating Fcs are in the normal range values when their disease, irrespective of its severity, is adequately controlled by the treatment they are receiving (Saunders et al, 2009;Bianchetti et al, 2012a; (Table 1). Greatly elevated blood Fc numbers are detectable in patients experiencing a spontaneous asthma exacerbation (Bellini et al, 2012;Isgrò et al, 2013a;Wang et al, 2015) and in patients with treatment-refractory severe disease (Saunders et al, 2009;Bianchetti et al, 2012a; or "chronic obstructive asthma" (Wang et al, 2008;2015), whose disease is scarcely controlled in spite of the intensive treatment with high doses of inhaled corticosteroids or oral corticosteroids in combination with bronchodilators (Table 1). Elevated numbers of circulating Fcs are consistently associated with the presence of airway (Saunders et al, 2009) or sputum fibrocytosis (Bellini et al, 2012) and ongoing inflammation, as reflected by sputum eosinophilia (Saunders et al, 2009;Bellini et al, 2012) and increased concentrations of proinflammatory cytokines and chemokines in the sputum fluid phase (Bellini et al, 2012;Isgrò et al, 2013b).…”

Section: Prognostic Roles In Asthmamentioning

confidence: 99%

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Pathogenetic and prognostic roles of bloodborne fibrocytes in asthma

Mattoli

2015

J. Zhejiang Univ. Sci. B

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Abstract:Bloodborne fibrocytes are cells mobilized from the bone marrow, which express surface antigens commonly ascribed to hematopoietic progenitors and have phenotypic and functional characteristics similar to those of immature mesenchymal cells. They exhibit predominant proinflammatory or profibrotic activities at tissue sites, depending on the host's response to environmental insults and on the characteristics of the cell infiltrate and cytokine milieu. In patients with allergic asthma, fibrocytes egress from the bone marrow and are recruited into the airways after every allergen exposure and during viral infections. Recruited fibrocytes amplify the inflammatory responses driven by T helper type 2 lymphokines and favor viral replication and further inflammation on respiratory virus infections. Persistently elevated blood fibrocyte counts and persisting airway fibrocytosis are present in patients with chronically undertreated or corticosteroid-insensitive asthma, and are linked to an enhanced risk of adverse outcomes because of the major involvement of fibrocytes in the development of structural abnormalities that lead to chronic airflow obstruction in these patients. Consequently, blood fibrocyte count is an emerging biomarker of asthma control and disease progression and its clinical applicability as a new outcome measure deserves further evaluation in large clinical trials.

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“…Researches from patients showed that circulating fibrocyte increased in various lung disease including chronic obstructive asthma 25 , acute asthma exacerbation without airflow obstruction 59 , acute exacerbation of chronic obstructive pulmonary disease (AECOPD) 60 , Fibrotic interstitial lung diseases 57 , IPF 61 , AECOPD 60 chronic hypersensitivity pneumonitis 62 , obliterative bronchiolitis (OB) 63 , cystic fibrosis patients 64 , rheumatoid arthritis-usual interstitial pneumonia 65 , pulmonary hypertension (PE) 66 , sickle cell lung disease 67 . Blood fibrocytes are recruited in lungs during COPD exacerbations and related to mortality and low lung function 60 .…”

Section: Clinical Pathogenic Significance Of Circulating Fibrocytementioning

confidence: 99%

Role of CXCL12/CXCR4-Mediated Circulating Fibrocytes in Pulmonary Fibrosis

Xie¹,

Zhao²

2017

J. Biomed

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Pulmonary fibrosis is characterized by excessive deposition of extracellular matrix (ECM) and remodeling of the lung architecture, with clinically irreversible loss of lung function. The exact molecular and cellular mechanisms of pulmonary fibrosis are complicated. Many types of cells are involved in the pathogenic processes. The chemokine (C-X-C motif) ligand 12 (CXCL12) can attract circulating fibrocytes trafficking into lungs via chemokine (C-X-C motif) receptor 4 (CXCR4) to promote tissue repair or impertinently worsen fibrotic lesions. In this review, we briefly summarize the existing experimental and clinical findings about fibrocytes in pulmonary fibrosis and discuss the potential therapeutic target CXCL12/CXCR4 biological axis.

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Fibrocyte trafficking in patients with chronic obstructive asthma and during an acute asthma exacerbation

Cited by 44 publications

References 29 publications

Current and future biomarkers in allergic asthma

Current and future biomarkers in allergic asthma

Pathogenetic and prognostic roles of bloodborne fibrocytes in asthma

Role of CXCL12/CXCR4-Mediated Circulating Fibrocytes in Pulmonary Fibrosis

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