Increased levels of soluble interleukin-6 receptor and CCL3 in COPD sputum

Ravi, Arjun; Khurana, Shruti; Lemon, J.E.; Plumb, Jonathan; Booth, George H.; Healy, Louise; Catley, Matthew C.; Vestbo, Jørgen; Singh, Dave

doi:10.1186/s12931-014-0103-4

Cited by 52 publications

(37 citation statements)

References 42 publications

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“…Recent reports have corroborated previous findings that neutrophils are increased in sputum of patients with COPD along with increased interleukin-6 (IL-6) signaling [59]. Substantial evidence has implicated primary or active smoking as a major contributor to the recruitment of these neutrophils; however, mounting evidence now suggests that secondhand smoke may have a similar effect on neutrophils [60] that is likely mediated through similar interleukin signaling [61,62].…”

Section: Health Outcomes and Comorbiditiesmentioning

confidence: 54%

Plausible Roles for RAGE in Conditions Exacerbated by Direct and Indirect (Secondhand) Smoke Exposure

Lewis

Hirschi

Arroyo

et al. 2017

IJMS

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Approximately 1 billion people smoke worldwide, and the burden placed on society by primary and secondhand smokers is expected to increase. Smoking is the leading risk factor for myriad health complications stemming from diverse pathogenic programs. First-and second-hand cigarette smoke contains thousands of constituents, including several carcinogens and cytotoxic chemicals that orchestrate chronic inflammatory responses and destructive remodeling events. In the current review, we outline details related to compromised pulmonary and systemic conditions related to smoke exposure. Specifically, data are discussed relative to impaired lung physiology, cancer mechanisms, maternal-fetal complications, cardiometabolic, and joint disorders in the context of smoke exposure exacerbations. As a general unifying mechanism, the receptor for advanced glycation end-products (RAGE) and its signaling axis is increasingly considered central to smoke-related pathogenesis. RAGE is a multi-ligand cell surface receptor whose expression increases following cigarette smoke exposure. RAGE signaling participates in the underpinning of inflammatory mechanisms mediated by requisite cytokines, chemokines, and remodeling enzymes. Understanding the biological contributions of RAGE during cigarette smoke-induced inflammation may provide critically important insight into the pathology of lung disease and systemic complications that combine during the demise of those exposed.

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Section: Health Outcomes and Comorbiditiesmentioning

confidence: 54%

Plausible Roles for RAGE in Conditions Exacerbated by Direct and Indirect (Secondhand) Smoke Exposure

Lewis

Hirschi

Arroyo

et al. 2017

IJMS

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“…Therefore, it appears likely that, under inflammatory conditions in the lung, increased levels of several shedding products are found in the alveolar fluid. In fact, this has been described for CX3CL1, JAM-A, CXCL16, TNF, TNFR, TGF-␣, IL6R, and syndecans in human sputum samples (20,89,123,153,198) or murine alveolar lavage fluid (32,33,148).…”

Section: Adam17mentioning

confidence: 72%

ADAM-family metalloproteinases in lung inflammation: potential therapeutic targets

Dreymueller

Uhlig

Ludwig

2015

American Journal of Physiology-Lung Cellular and Molecular Phys

121

107

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-Acute and chronic lung inflammation is driven and controlled by several endogenous mediators that undergo proteolytic conversion from surface-expressed proteins to soluble variants by a disintegrin and metalloproteinase (ADAM)-family members. TNF and epidermal growth factor receptor ligands are just some of the many substrates by which these proteases regulate inflammatory or regenerative processes in the lung. ADAM10 and ADAM17 are the most prominent members of this protease family. They are constitutively expressed in most lung cells and, as recent research has shown, are the pivotal shedding enzymes mediating acute lung inflammation in a cell-specific manner. ADAM17 promotes endothelial and epithelial permeability, transendothelial leukocyte migration, and inflammatory mediator production by smooth muscle and epithelial cells. ADAM10 is critical for leukocyte migration and alveolar leukocyte recruitment. ADAM10 also promotes allergic asthma by driving B cell responses. Additionally, ADAM10 acts as a receptor for Staphylococcus aureus (S. aureus) ␣-toxin and is crucial for bacterial virulence. ADAM8, ADAM9, ADAM15, and ADAM33 are upregulated during acute or chronic lung inflammation, and recent functional or genetic analyses have linked them to disease development. Pharmacological inhibitors that allow us to locally or systemically target and differentiate ADAM-family members in the lung suppress acute and asthmatic inflammatory responses and S. aureus virulence. These promising results encourage further research to develop therapeutic strategies based on selected ADAMs. These studies need also to address the role of the ADAMs in repair and regeneration in the lung to identify further therapeutic opportunities and possible side effects. metalloproteinase; shedding; inflammation; edema; asthma ACUTE OR CHRONIC INFLAMMATION in the lung can lead to a fatal loss of lung functions. Acute inflammation resulting from infection, aspiration of gastric juice, or overventilation during intensive care is initially characterized by enhanced inflammatory mediator production, edema formation, and recruitment of innate immune cells with the risk of lung damage. Asthma, chronic obstructive pulmonary disease (COPD), and lung fibrosis are fatal chronic diseases that are driven by persistent inflammation with a lack of resolution and impaired tissue regeneration. Targeting the immune response is the underlying principle of many treatment strategies against these diseases (reviewed in Ref. 7).The cytokines, growth factors, receptors, and adhesion molecules that drive the inflammatory process are all under intensive scrutiny. Many of these molecules undergo functional modulation by limited proteolysis, bringing the participating proteases into the focus of attention. Among these proteases is a class of metalloproteinases that subdivides into the matrix metalloproteinases (MMP) and the families of a disintegrin and metalloproteinases (ADAM) and ADAM with trombospondin motif. MMPs have already been intensively investigated with resp...

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“…Sputum IL-6 level is increased in asthma and COPD compared to healthy subjects. 16 IL-6 has been shown to play a particular role in COPD: Elevated concentrations of it correlate with impaired lung function and are related to high frequencies of COPD exacerbations. 17 On the other hand, IL-13 is described as one of the key mediators of allergic asthma, promoting eosinophil predominance, goblet cell hyperplasia and mucus hypersecretion in the respiratory tract.…”

Section: -14mentioning

confidence: 99%

A comparative study of sTREM-1, IL-6 and IL-13 concentration in bronchoalveolar lavage fluid in asthma and COPD: A preliminary study

Proboszcz¹,

Paplińska-Goryca²,

Nejman-Gryz³

et al. 2017

Adv Clin Exp Med

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Background. Soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) is a cell-surface receptor presented on neutrophils, macrophages and monocytes. Elevated sTREM-1 levels are a marker of acute microbial infections, and have also been reported in chronic lung diseases. IL-6 and IL-13 are effective markers in distinguishing these diseases. IL-6 has been shown to play an important role in chronic obstructive pulmonary disease (COPD), while IL-13 is described as one of the key mediators of allergic asthma.

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Increased levels of soluble interleukin-6 receptor and CCL3 in COPD sputum

Cited by 52 publications

References 42 publications

Plausible Roles for RAGE in Conditions Exacerbated by Direct and Indirect (Secondhand) Smoke Exposure

Plausible Roles for RAGE in Conditions Exacerbated by Direct and Indirect (Secondhand) Smoke Exposure

ADAM-family metalloproteinases in lung inflammation: potential therapeutic targets

A comparative study of sTREM-1, IL-6 and IL-13 concentration in bronchoalveolar lavage fluid in asthma and COPD: A preliminary study

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