Fibrocyte localization to the airway smooth muscle is a feature of asthma

Saunders, Ruth; Siddiqui, Salman; Kaur, Davinder; Doe, Camille; Sutcliffe, Amanda; Hollins, Fay; Bradding, Peter; Wardlaw, Andrew J.; Brightling, Christopher E.

doi:10.1016/j.jaci.2008.10.048

Cited by 114 publications

(185 citation statements)

References 39 publications

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“…Second, autopsy and biopsy studies have linked an increased amount of airway smooth muscle to asthma severity, airflow obstruction and bronchial hyperresponsiveness [71,[106][107][108][109]. Finally, fibrocytes, which can differentiate into myofibroblasts, are increased in blood and in smooth muscle bundles in asthmatics with fixed airways obstruction and/or severe asthma [110,111].…”

Section: Structural Abnormalitiesmentioning

confidence: 99%

International ERS/ATS guidelines on definition, evaluation and treatment of severe asthma

et al. 2013

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Severe or therapy-resistant asthma is increasingly recognised as a major unmet need. A Task Force, supported by the European Respiratory Society and American Thoracic Society, reviewed the definition and provided recommendations and guidelines on the evaluation and treatment of severe asthma in children and adults.A literature review was performed, followed by discussion by an expert committee according to the GRADE (Grading of Recommendations, Assessment, Development and Evaluation) approach for development of specific clinical recommendations.When the diagnosis of asthma is confirmed and comorbidities addressed, severe asthma is defined as asthma that requires treatment with high dose inhaled corticosteroids plus a second controller and/or systemic corticosteroids to prevent it from becoming “uncontrolled” or that remains “uncontrolled” despite this therapy. Severe asthma is a heterogeneous condition consisting of phenotypes such as eosinophilic asthma. Specific recommendations on the use of sputum eosinophil count and exhaled nitric oxide to guide therapy, as well as treatment with anti-IgE antibody, methotrexate, macrolide antibiotics, antifungal agents and bronchial thermoplasty are provided.Coordinated research efforts for improved phenotyping will provide safe and effective biomarker-driven approaches to severe asthma therapy.

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Section: Structural Abnormalitiesmentioning

confidence: 99%

International ERS/ATS guidelines on definition, evaluation and treatment of severe asthma

et al. 2013

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“…In this study, there was an inverse correlation between the number of interstitial fibrocytes and kidney function. In addition, fibrocytes numbers in peripheral blood have been reported to predict early mortality in patients with idiopathic pulmonary fibrosis and increase in accordance with the severity of asthma [23,35]. Taken together, these observations suggest that the number of fibrocytes in clinical samples may be useful as a biomarker for the progression of organ fibrosis.…”

mentioning

confidence: 73%

“…In addition, the extent of fibrocyte infiltration into the bronchial mucosa increases in accordance with the severity of persistent airflow obstruction [23]. In fibrotic conditions, the signaling of fibrogenic cytokines such as TGF-β 1 has been shown to be involved in the pathogenesis of organ fibrosis, including human kidney disease [25].…”

Section: Discussionmentioning

confidence: 99%

Fibrocytes are involved in the pathogenesis of human chronic kidney disease

et al. 2010

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“…Tissue fibrosis (4), inappropriate angiogenesis (5), cancer cell metastasis (6), and increased airway smooth muscle mass in asthma (7) are a few examples of progressively disproportionate cell migration. Attempts have been made to understand the source of migrating cells (8)(9)(10)(11)(12) with the hope of better understanding the role of migration in diseases such as asthma, where the origins of migrating cells are not known in vivo (13) and, hence, cannot be specifically targeted. However, regardless of the origins of migrating cells, active recruitment of cells from different sites, near or far, is central for disease chronicity and severity (8,14).…”

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confidence: 99%

CXCL1 Inhibits Airway Smooth Muscle Cell Migration through the Decoy Receptor Duffy Antigen Receptor for Chemokines

Al-Alwan

Chang

Rousseau

et al. 2014

The Journal of Immunology

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Airway smooth muscle cell (ASMC) migration is an important mechanism postulated to play a role in airway remodeling in asthma. CXCL1 chemokine has been linked to tissue growth and metastasis. In this study, we present a detailed examination of the inhibitory effect of CXCL1 on human primary ASMC migration and the role of the decoy receptor, Duffy AgR for chemokines (DARC), in this inhibition. Western blots and pathway inhibitors showed that this phenomenon was mediated by activation of the ERK-1/2 MAPK pathway, but not p38 MAPK or PI3K, suggesting a biased selection in the signaling mechanism. Despite being known as a nonsignaling receptor, small interference RNA knockdown of DARC showed that ERK-1/2 MAPK activation was significantly dependent on DARC functionality, which, in turn, was dependent on the presence of heat shock protein 90 subunit α. Interestingly, DARC- or heat shock protein 90 subunit α–deficient ASMCs responded to CXCL1 stimulation by enhancing p38 MAPK activation and ASMC migration through the CXCR2 receptor. In conclusion, we demonstrated DARC’s ability to facilitate CXCL1 inhibition of ASMC migration through modulation of the ERK-1/2 MAPK–signaling pathway.

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Fibrocyte localization to the airway smooth muscle is a feature of asthma

Abstract: Background-Airway smooth muscle (ASM) hyperplasia is a hallmark of asthma that is associated with disease severity and persistent airflow obstruction.

Cited by 114 publications

References 39 publications

International ERS/ATS guidelines on definition, evaluation and treatment of severe asthma

International ERS/ATS guidelines on definition, evaluation and treatment of severe asthma

Fibrocytes are involved in the pathogenesis of human chronic kidney disease

CXCL1 Inhibits Airway Smooth Muscle Cell Migration through the Decoy Receptor Duffy Antigen Receptor for Chemokines

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