Circulating Secretoglobin Family 1A Member 1 (SCGB1A1) Levels as a Marker of Biomass Smoke Induced Chronic Obstructive Pulmonary Disease

Veerapaneni, Vivek Vardhan; Upadhyay, Swapna; Thimraj, Tania A.; Siddaiah, Jayaraj Biligere; Krishnarao, Chaya Sindaghatta; Lokesh, Komarla Sundararaja; Thimmulappa, Rajesh K.; Palmberg, Lena; Ganguly, Koustav; Anand, Mahesh Padukudru

doi:10.3390/toxics9090208

Cited by 4 publications

(1 citation statement)

References 38 publications

(77 reference statements)

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“…Serum levels of secretoglobin family 1A member 1 (SCGB1A1) also known as club cell protein 16 or CC16, were lower in both the BS-COPD and CS-COPD compared to the CS controls and healthy controls. In addition, the SCGB1A1 levels were positively correlated with FEV1, FVC, and exercise capacity [148].…”

Section: Inflammationmentioning

confidence: 88%

Mechanisms of Lung Damage and Development of COPD Due to Household Biomass-Smoke Exposure: Inflammation, Oxidative Stress, MicroRNAs, and Gene Polymorphisms

Ortiz‐Quintero

Martinez-Espinosa

Pérez‐Padilla

2022

Cells

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Chronic exposure to indoor biomass smoke from the combustion of solid organic fuels is a major cause of disease burden worldwide. Almost 3 billion people use solid fuels such as wood, charcoal, and crop residues for indoor cooking and heating, accounting for approximately 50% of all households and 90% of rural households globally. Biomass smoke contains many hazardous pollutants, resulting in household air pollution (HAP) exposure that often exceeds international standards. Long-term biomass-smoke exposure is associated with Chronic Obstructive Pulmonary Disease (COPD) in adults, a leading cause of morbidity and mortality worldwide, chronic bronchitis, and other lung conditions. Biomass smoke-associated COPD differs from the best-known cigarette smoke-induced COPD in several aspects, such as a slower decline in lung function, greater airway involvement, and less emphysema, which suggests a different phenotype and pathophysiology. Despite the high burden of biomass-associated COPD, the molecular, genetic, and epigenetic mechanisms underlying its pathogenesis are poorly understood. This review describes the pathogenic mechanisms potentially involved in lung damage, the development of COPD associated with wood-derived smoke exposure, and the influence of genetic and epigenetic factors on the development of this disease.

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Section: Inflammationmentioning

confidence: 88%

Mechanisms of Lung Damage and Development of COPD Due to Household Biomass-Smoke Exposure: Inflammation, Oxidative Stress, MicroRNAs, and Gene Polymorphisms

Ortiz‐Quintero

Martinez-Espinosa

Pérez‐Padilla

2022

Cells

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Clara cell 10 (CC10) protein attenuates allergic airway inflammation by modulating lung dendritic cell functions

Xu,

Cheng,

Mao

et al. 2024

Cell. Mol. Life Sci.

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Allergic asthma is a complex inflammatory disorder predominantly orchestrated by T helper 2 (Th2) lymphocytes. The anti-inflammatory protein Clara Cell 10-kDa (CC10), also known as secretoglobin family 1A member 1 (SCGB1A1), shows promise in modulating respiratory diseases. However, its precise role in asthma remains unclear. This study examines the potential of CC10 to suppress allergic asthma inflammation, specifically assessing its regulatory effects on Th2 cell responses and dendritic cells (DCs). Lower CC10 levels in asthma were observed and correlated with increased IgE and lymphocytes. Cc10−/− mice exhibited exacerbated allergic airway inflammation marked by increased inflammatory cell infiltration, Th2 cytokines, serum antigen-specific IgE levels, and airway hyperresponsiveness (AHR) in house dust mite (HDM)-induced models. Conversely, recombinant CC10 significantly attenuated these inflammatory responses. Intriguingly, CC10 did not directly inhibit Th cell activation but significantly downregulated the population of CD11b+CD103− DCs subsets in lungs of asthmatic mice and modulated the immune activation functions of DCs through NF-κB signaling pathway. The mixed lymphocyte response assay revealed that DCs mediated the suppressive effect of CC10 on Th2 cell responses. Collectively, CC10 profoundly mitigates Th2-type allergic inflammation in asthma by modulating lung DC phenotype and functions, highlighting its therapeutic potential for inflammatory airway conditions and other related immunological disorders.

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Lung Organoids: Systematic Review of Recent Advancements and its Future Perspectives

Thangam,

Parthasarathy,

Supraja

et al. 2024

Tissue Eng Regen Med

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Circulating Secretoglobin Family 1A Member 1 (SCGB1A1) Levels as a Marker of Biomass Smoke Induced Chronic Obstructive Pulmonary Disease

Cited by 4 publications

References 38 publications

Mechanisms of Lung Damage and Development of COPD Due to Household Biomass-Smoke Exposure: Inflammation, Oxidative Stress, MicroRNAs, and Gene Polymorphisms

Mechanisms of Lung Damage and Development of COPD Due to Household Biomass-Smoke Exposure: Inflammation, Oxidative Stress, MicroRNAs, and Gene Polymorphisms

Clara cell 10 (CC10) protein attenuates allergic airway inflammation by modulating lung dendritic cell functions

Lung Organoids: Systematic Review of Recent Advancements and its Future Perspectives

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