IL-36 Cytokines Promote Inflammation in the Lungs of Long-Term Smokers

Kovach, Melissa A.; Che, Karlhans; Brundin, Bettina; Andersson, Anders; Ásgeirsdóttir, Helga; Padra, Médea; Lindén, Sara K.; Qvarfordt, Ingemar; Newstead, Michael W.; Standiford, Theodore J.; Lindén, Anders

doi:10.1165/rcmb.2020-0035oc

Cited by 19 publications

(21 citation statements)

References 46 publications

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“…The role of IL-36 cytokines in the lungs is not restricted to infectious diseases. Studies have described a potentially important role of the IL-36 pathway in asthma ( 98 , 99 ), idiopathic pulmonary fibrosis ( 21 , 100 ), chronic obstructive pulmonary disease ( 101 , 102 ), cystic fibrosis ( 103 ) and cancer ( 104 ). During asthma, the levels of the anti-inflammatory IL36Ra in the serum and sputum of asthmatic patients are reduced compared to healthy controls ( 98 ).…”

Section: The Active Role Of Il-36 Cytokines During Lung Inflammatory Diseasesmentioning

confidence: 99%

“…Promising data regarding the role of IL-36 cytokines in the development and severity of COPD has emerged in the last years. Studies have demonstrated that normal human bronchial epithelial cells and primary human bronchial epithelial cells express high amounts of IL-36α, IL-36β, IL-36γ and IL-36Ra after being treated with cigarette smoke components – a causative agent of COPD – in vitro ( 101 , 102 ). Moreover, smokers with and without COPD presented with elevated levels of IL-36α, and IL-36γ in plasma and BALF at baseline, although no differences in IL-36 cytokines levels were found between non-COPD smokers and COPD smokers ( 102 ).…”

Section: The Active Role Of Il-36 Cytokines During Lung Inflammatory Diseasesmentioning

confidence: 99%

“…Studies have demonstrated that normal human bronchial epithelial cells and primary human bronchial epithelial cells express high amounts of IL-36α, IL-36β, IL-36γ and IL-36Ra after being treated with cigarette smoke components – a causative agent of COPD – in vitro ( 101 , 102 ). Moreover, smokers with and without COPD presented with elevated levels of IL-36α, and IL-36γ in plasma and BALF at baseline, although no differences in IL-36 cytokines levels were found between non-COPD smokers and COPD smokers ( 102 ). Another study showed that IL-36α, and IL-36γ were increased in the sputum of neutrophilic COPD patients, compared to eosinophilic COPD, and were associated with the amount of neutrophils in the sputum ( 106 ).…”

Section: The Active Role Of Il-36 Cytokines During Lung Inflammatory Diseasesmentioning

confidence: 99%

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Interleukin-36 Cytokines in Infectious and Non-Infectious Lung Diseases

et al. 2021

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The IL-36 family of cytokines were identified in the early 2000’s as a new subfamily of the IL-1 cytokine family, and since then, the role of IL-36 cytokines during various inflammatory processes has been characterized. While most of the research has focused on the role of these cytokines in autoimmune skin diseases such as psoriasis and dermatitis, recent studies have also shown the importance of IL-36 cytokines in the lung inflammatory response during infectious and non-infectious diseases. In this review, we discuss the biology of IL-36 cytokines in terms of how they are produced and activated, as well as their effects on myeloid and lymphoid cells during inflammation. We also discuss the role of these cytokines during lung infectious diseases caused by bacteria and influenza virus, as well as other inflammatory conditions in the lungs such as allergic asthma, lung fibrosis, chronic obstructive pulmonary disease, cystic fibrosis and cancer. Finally, we discuss the current therapeutic advances that target the IL-36 pathway and the possibility to extend these tools to treat lung inflammatory diseases.

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Section: The Active Role Of Il-36 Cytokines During Lung Inflammatory Diseasesmentioning

confidence: 99%

Section: The Active Role Of Il-36 Cytokines During Lung Inflammatory Diseasesmentioning

confidence: 99%

Section: The Active Role Of Il-36 Cytokines During Lung Inflammatory Diseasesmentioning

confidence: 99%

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Interleukin-36 Cytokines in Infectious and Non-Infectious Lung Diseases

et al. 2021

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“…Airway inflammation is one of the characteristic pathological changes observed in CS and infection-induced diseases (i.e., AECOPD). Both CS and viral infections lead to lung inflammatory responses, which include recruitment of immune cells into the airway, the release of proinflammatory cytokines, and an oxidant-antioxidant imbalance [36][37][38]. Infection with respiratory pathogens such as rhinovirus, influenza virus, and coronavirus reportedly aggravates inflammation in CS-exposed lungs [39,40].…”

Section: Discussionmentioning

confidence: 99%

The traditional herbal formulation, Jianpiyifei II, reduces pulmonary inflammation induced by influenza A virus and cigarette smoke in mice

Cai

Liu

et al. 2021

Clinical Science

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Chronic obstructive pulmonary disease (COPD) is a worldwide chronic inflammatory lung disease, and influenza A virus (IAV) infection is a common cause of acute exacerbations of COPD (AECOPD). Therefore, targeting viral infections represents a promising strategy to prevent the occurrence and development of inflammatory flare ups in AECOPD. Jianpiyifei II (JPYFII) is a traditional herbal medicine used in China to treat patients with COPD, and its clinical indications are not well understood. However, investigation of the anti-inflammatory effects and underlying mechanism using an animal model of smoking has been reported in a previous study by our group. In addition, some included herbs, such as Radix astragali and Radix aupleuri, were reported to exhibit anti-viral effects. Therefore, the aim of this study was to investigate whether JPYFII formulation relieved acute inflammation by clearing the IAV in a mouse model that was exposed to cigarette smoke experimentally. JPYFII formulation treatment during smoke exposure and IAV infection significantly reduced the number of cells observed in bronchoalveolar lavage fluid (BALF), expression of pro-inﬂammatory cytokines, chemokines, superoxide production, and viral load in IAV-infected and smoke-exposed mice. However, JPYFII formulation treatment during smoke exposure alone did not reduce the number of cells in BALF or the expression of Il-6, Tnf-a, and Il-1β. The results demonstrated that JPYFII formulation exerted an anti-viral effect and reduced the exacerbation of lung inflammation in cigarette smoke (CS)-exposed mice infected with IAV. Our results suggested that JPYFII formulation could potentially be used to treat patients with AECOPD associated with IAV infection.

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“…Similarly, a role for IL-36 in promoting a pro-inflammatory environment in the lungs of long-term smokers with and without COPD has been identified. IL-36α and IL-36γ are enhanced systemically and locally in long-term smokers with and without COPD, and local IL-36α concentrations display a positive correlation with declining ventilatory lung function and increasing pro-inflammatory cytokine concentrations [ 77 ]. Mechanistically, at least some of the pathogenic effect of IL-36 in the lung appears to be via recruitment of neutrophils.…”

Section: The Role Of Il-36 In the Pathogenesis Of Inflammatory Diseasesmentioning

confidence: 99%

IL-36 cytokines in inflammatory and malignant diseases: not the new kid on the block anymore

Byrne

Baker

Houston

et al. 2021

Cell. Mol. Life Sci.

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The IL-36 family of cytokines were first identified in 2000 based on their sequence homology to IL-1 cytokines. Over subsequent years, the ability of these cytokines to either agonise or antagonise an IL-1R homologue, now known as the IL-36 Receptor (IL-36R), was identified and these cytokines went through several cycles of renaming with the current nomenclature being proposed in 2010. Despite being identified over 20 years ago, it is only during the last decade that the function of these cytokines in health and disease has really begun to be appreciated, with both homeostatic functions in wound healing and response to infection, as well as pathological functions now ascribed. In the disease context, over activation of IL-36 has now been associated with many inflammatory diseases including Psoriasis and inflammatory bowel diseases, with roles in cancer also now being investigated. This review summarises the current knowledge of IL-36 biology, its role in inflammatory diseases and focuses on an emerging role for IL-36 in cancer.

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IL-36 Cytokines Promote Inflammation in the Lungs of Long-Term Smokers

Cited by 19 publications

References 46 publications

Interleukin-36 Cytokines in Infectious and Non-Infectious Lung Diseases

Interleukin-36 Cytokines in Infectious and Non-Infectious Lung Diseases

The traditional herbal formulation, Jianpiyifei II, reduces pulmonary inflammation induced by influenza A virus and cigarette smoke in mice

IL-36 cytokines in inflammatory and malignant diseases: not the new kid on the block anymore

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