Airway Inflammation and Inflammatory Biomarkers

Lim, Hui Fang; Nair, Parameswaran

doi:10.1055/s-0037-1606217

Cited by 31 publications

(22 citation statements)

References 93 publications

(85 reference statements)

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“…Perceived difficulties in implementing this approach in routine clinical practice have limited its widespread use. In fact, as described by Lim and Nair ( 12 ), many easily accessible biomarkers with demonstrated clinical utility remain confined to the research arena or are only exploited in a small number of specialized academic centers. This may be due to the lack of measurement standardization, validated diagnostic or predictive thresholds, and evidence-based reference guidelines to inform how biomarkers should be used and interpreted in clinical practice.…”

Section: Inflammatory Endotypesmentioning

confidence: 99%

Asthma Endotypes and an Overview of Targeted Therapy for Asthma

2017

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Guidelines for the management of severe asthma do not emphasize the measurement of the inflammatory component of airway disease to indicate appropriate treatments or to monitor response to treatment. Inflammation is a central component of asthma and contributes to symptoms, physiological, and structural abnormalities. It can be assessed by a number of endotyping strategies based on “omics” technology such as proteomics, transcriptomics, and metabolomics. It can also be assessed using simple cellular responses by quantitative cytometry in sputum. Bronchitis may be eosinophilic, neutrophilic, mixed-granulocytic, or paucigranulocytic (eosinophils and neutrophils not elevated). Eosinophilic bronchitis is usually a Type 2 (T2)-driven process and therefore a sputum eosinophilia of greater than 3% usually indicates a response to treatment with corticosteroids or novel therapies directed against T2 cytokines such as IL-4, IL-5, and IL-13. Neutrophilic bronchitis represents a non-T2-driven disease, which is generally a predictor of response to antibiotics and may be a predictor to therapies targeted at pathways that lead to neutrophil recruitment such as TNF, IL-1, IL-6, IL-8, IL-23, and IL-17. Paucigranulocytic disease may not warrant anti-inflammatory therapy. These patients, whose symptoms may be driven largely by airway hyper-responsiveness may benefit from smooth muscle-directed therapies such as bronchial thermoplasty or mast-cell directed therapies. This review will briefly summarize the current knowledge regarding “omics-based signatures” and cellular endotyping of severe asthma and give an overview of segmentation of asthma therapeutics guided by the endotype.

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Section: Inflammatory Endotypesmentioning

confidence: 99%

Asthma Endotypes and an Overview of Targeted Therapy for Asthma

2017

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“…T2-high airway inflammation drives the transcription of inducible NOS (iNOS), thus increasing NO production. FeNO predominantly signifies IL-4 and IL-13 activity, with FeNO concentrations greater than 50 ppb (> 35 ppb in children) alluding to eosinophilic airway inflammation and steroid responsiveness [56]. Thus, the role of FeNO may be additive as a biomarker in relation to asthma morbidity.…”

Section: Introductionmentioning

confidence: 99%

Understanding Asthma Phenotypes, Endotypes, and Mechanisms of Disease

Kuruvilla

Lee

2018

Clinic Rev Allerg Immunol

833

719

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The model of asthma as a single entity has now been replaced by a much more complex biological network of distinct and interrelating inflammatory pathways. The term asthma is now considered an umbrella diagnosis for several diseases with distinct mechanistic pathways (endotypes) and variable clinical presentations (phenotypes). The precise definition of these endotypes is central to asthma management due to inherent therapeutic and prognostic implications. This review presents the molecular mechanisms behind the heterogeneity of airway inflammation in asthmatic patients. Asthma endotypes may be broadly regarded as type 2 (T2) high or T2-low. Several biologic agents have been approved for T2-high asthma, with numerous other therapeutics that are incipient and similarly targeted at specific molecular mechanisms. Collectively, these advances have shifted existing paradigms in the approach to asthma to tailor novel therapies.

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“…Thus, there remains an unmet clinical need in the study of the mechanisms and biomarkers for both T2-high and T2-low endotypes as concerns their ability to predict response to targeted therapy (22). The development of solid biomarkers combined with a deeper understanding of the pathology and physiology of asthma will allow a more direct and effective treatment of asthmatic patients through approaches based on precision medicine (23).…”

Section: Introductionmentioning

confidence: 99%

Discriminatory Molecular Biomarkers of Allergic and Nonallergic Asthma and Its Severity

et al. 2019

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Asthma is a complex disease comprising various phenotypes and endotypes, all of which still need solid biomarkers for accurate classification. In a previous study, we defined specific genes related to asthma and respiratory allergy by studying the expression of 94 genes in a population composed of 4 groups of subjects: healthy control, nonallergic asthmatic, asthmatic allergic, and nonasthmatic allergic patients. An analysis of differential gene expression between controls and patients revealed a set of statistically relevant genes mainly associated with disease severity, i.e., CHI3L1, IL-8, IL-10, MSR1, PHLDA1, PI3 , and SERPINB2 . Here, we analyzed whether these genes and their proteins could be potential asthma biomarkers to distinguish between nonallergic asthmatic and asthmatic allergic subjects. Protein quantification was determined by ELISA (in serum) or Western blot (in protein extracted from peripheral blood mononuclear cells or PBMCs). Statistical analyses were performed by unpaired t -test using the Graph-Pad program. The sensitivity and specificity of the gene and protein expression of several candidate biomarkers in differentiating the two groups (and the severity subgroups) was performed by receiver operating characteristic (ROC) curve analysis using the R program. The ROC curve analysis determined single genes with good sensitivity and specificity for discriminating some of the phenotypes. However, interesting combinations of two or three protein biomarkers were found to distinguish the asthma disease and disease severity between the different phenotypes of this pathology using reproducible techniques in easy-to-obtain samples. Gene and protein panels formed by single biomarkers and biomarker combinations have been defined in easily obtainable samples and by standardized techniques. These panels could be useful for characterizing phenotypes of asthma, specifically when differentiating asthma severity.

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Airway Inflammation and Inflammatory Biomarkers

Cited by 31 publications

References 93 publications

Asthma Endotypes and an Overview of Targeted Therapy for Asthma

Asthma Endotypes and an Overview of Targeted Therapy for Asthma

Understanding Asthma Phenotypes, Endotypes, and Mechanisms of Disease

Discriminatory Molecular Biomarkers of Allergic and Nonallergic Asthma and Its Severity

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