Cigarette smoke affects IL-17A, IL-17F and IL-17 receptor expression in the lung tissue: Ex vivo and in vitro studies

Montalbano, Angela Marina; Riccobono, Loredana; Siena, Liboria; Chiappara, Giuseppina; Sano, Caterina Di; Anzalone, Giulia; Gagliardo, Rosalia; Ricciardolo, Fabio Luigi Massimo; Sorbello, Valentina; Pipitone, Loredana; Vitulo, Patrizio; Profita, Mirella

doi:10.1016/j.cyto.2015.07.013

Cited by 42 publications

(30 citation statements)

References 39 publications

(40 reference statements)

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“…Moreover, CS also influences DC function by altering their capability to produce prostaglandin-E2, IL-8, and IL-10, as well as suppressing the release of IL-12 and IL-23 (41). While CSE has been shown to increase expression of IL-17A and IL-17 receptor in the lung tissue (19) and certain individuals with chronic CS exposure have increased Th17 immunity (42), our data show that direct CSE exposure is not leading to Th17 polarization. This was shown by a reversed ability of Th CSE cells to produce IL-17 and IL-2.…”

Section: Discussioncontrasting

confidence: 49%

“…Components of CS and CSE contain a large number of chemicals, many of which have cancerogenic properties (18) and trigger AhR signaling in the cells. Although AhR stimulation is directly involved in the development of Th17 and CS has been shown to increase IL-17A and IL-17F expression in lungs, little is known about the direct effect of CS components on the development of Th17 cells (3, 19). To address this, we tested the effect of CSE on Th17 cell polarization upon stimulation of the TCR/CD3 complex and in the presence of standard cytokines used for Th17 differentiation (20).…”

Section: Resultsmentioning

confidence: 99%

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Th17 Polarization under Hypoxia Results in Increased IL-10 Production in a Pathogen-Independent Manner

et al. 2017

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The IL-17-producing CD4+ T helper cell (Th17) differentiation is affected by stimulation of the aryl hydrocarbon receptor (AhR) pathway and by hypoxia-inducible factor 1 alpha (HIF-1α). In some cases, Th17 become non-pathogenic and produce IL-10. However, the initiating events triggering this phenotype are yet to be fully understood. Here, we show that such cells may be differentiated at low oxygen and regardless of AhR ligand treatment such as cigarette smoke extract. Hypoxia led to marked alterations of the transcriptome of IL-10-producing Th17 cells affecting genes involved in metabolic, anti-apoptotic, cell cycle, and T cell functional pathways. Moreover, we show that oxygen regulates the expression of CD52, which is a cell surface protein that has been shown to suppress the activation of other T cells upon release. Taken together, these findings suggest a novel ability for Th17 cells to regulate immune responses in vivo in an oxygen-dependent fashion.

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Section: Discussioncontrasting

confidence: 49%

Section: Resultsmentioning

confidence: 99%

Th17 Polarization under Hypoxia Results in Increased IL-10 Production in a Pathogen-Independent Manner

et al. 2017

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“…And, melanocyte apoptosis is considered as a mechanism of depigmentation in vitiligo (Singh et al, 2016). In many in vitro experiments, IL-17F possesses the pro-inflammatory function, similar to IL-17A, contributing to host defense and autoimmune function of Th17 cells (Jie et al, 2014;Montalbano et al, 2015), indicating that IL-17F may play similar roles as IL-17A in vitiligo. In many in vitro experiments, IL-17F possesses the pro-inflammatory function, similar to IL-17A, contributing to host defense and autoimmune function of Th17 cells (Jie et al, 2014;Montalbano et al, 2015), indicating that IL-17F may play similar roles as IL-17A in vitiligo.…”

Section: Discussionmentioning

confidence: 99%

“…Besides, IL-17F, as a newly discovered member of IL-17 family, shares high homology with IL-17A (Chang & Dong, 2009). In many in vitro experiments, IL-17F possesses the pro-inflammatory function, similar to IL-17A, contributing to host defense and autoimmune function of Th17 cells (Jie et al, 2014;Montalbano et al, 2015), indicating that IL-17F may play similar roles as IL-17A in vitiligo. Moreover, the mRNA levels of RORgt and BATF in PBMC were also detected to be dramatically increased in PBMC of vitiligo patients in our research.…”

Section: Discussionmentioning

confidence: 99%

The expression change of RORγt, BATF, and IL‐17 in Chinese vitiligo patients with 308 nanometers excimer laser treatment

Wang

Zhang

Zhou

et al. 2018

Dermatologic Therapy

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This study aims to explore the expression of RORγt, BATF, and IL-17 in Chinese vitiligo patients with 308 nm excimer laser treatment. One hundred and sixty-four vitiligo patients treated with 308 nm excimer laser were enrolled as Case group and 137 health examiners as Control group. Quantitative real-time polymerase chain reaction and immunohistochemistry were conducted to detect the expressions of RORγt, BATF, and IL-17. Expression of RORγt, BATF, IL-17A, and IL-17F were higher in Case group than Control group, with the diagnostic accuracy of 88.04, 87.38, 97.34, and 89.04%, respectively. Pearson correlation analysis showed a positive correlation in RORγt, BATF, IL-17A, and IL-17F mRNAs in vitiligo patients. Moreover, their expressions were higher in active vitiligo patients than stable ones. Besides, the expressions of RORγt, BATF, IL-17A, and IL-17F in vitiligo skin were significantly higher than those in non lesional skin and normal controls. After treatment, their expressions were significantly decreased. Active vitiligo and the high expressions of RORγt, BATF, and IL-17F were the independent risk factors for the ineffectiveness of 308 nm excimer laser treatment. The expressions of RORγt, BATF, IL-17 were significantly enhanced in vitiligo patients, which were correlated with the activity of vitiligo and 308 nm excimer laser therapeutic effects.

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“…Clinical studies have also demonstrated an inverse correlation between increased frequencies of IL-17-producing cells or serum IL-17 levels and favorable patient prognosis (5)(6)(7). In addition, a strong link between smoking, enhanced innate inflammatory activity, and IL-17 production has been reported in both preclinical and clinical studies (8)(9)(10). Therefore, therapeutic strategies that are designed to block IL-17driven inflammation could represent an attractive strategy for the prevention and/or treatment of early-stage lung cancer.…”

mentioning

confidence: 95%

Inhaled IL-10 Suppresses Lung Tumorigenesis via Abrogation of Inflammatory Macrophage–Th17 Cell Axis

Anderson

Egilmez

2018

The Journal of Immunology

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Intratracheal administration of a novel IL-10 formulation suppressed IL-17–driven, CD4+ T cell–dependent tumorigenesis in the LSL-K-rasG12D murine lung cancer model. Analysis of lung lymphocyte populations demonstrated that antitumor activity of IL-10 was associated with a 5-fold decline in Th17 cell prevalence and a concurrent suppression of inflammatory M1-like macrophage activity. Further phenotypic characterization revealed that macrophages and dendritic cells, but not Th17 cells, expressed IL-10RA on the cell surface with the CD11b+F4/80+CX3CR1+ interstitial macrophages representing the dominant IL-10RA+ subset. Consistent with these observations, in vitro stimulation of sorted CD4+ T cells with IL-10 did not affect their ability to produce IL-17, whereas similar treatment of purified interstitial macrophages resulted in a dramatic M1 to M2 phenotypic switch. Importantly, preconditioning of macrophages (but not of CD4+ T cells) with IL-10 led to potent suppression of CD4+ T cell IL-17 production in an in vitro coculture assay, suggesting that IL-10 suppressed Th17 cell activity primarily via its upstream effects on macrophages. In support of this notion, in vivo macrophage depletion resulted in a 5-fold decline in Th17 cell numbers and a concurrent 6-fold reduction in tumor burden. Collectively, these data demonstrate that in the LSL-K-rasG12D murine lung cancer model, inflammatory macrophage–Th17 cell axis is critical to tumorigenesis and that IL-10 blocks this process primarily via a direct effect on the former. Inhaled IL-10 formulations may be of use in prophylaxis against lung cancer in high-risk patients.

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Cigarette smoke affects IL-17A, IL-17F and IL-17 receptor expression in the lung tissue: Ex vivo and in vitro studies

Cited by 42 publications

References 39 publications

Th17 Polarization under Hypoxia Results in Increased IL-10 Production in a Pathogen-Independent Manner

Th17 Polarization under Hypoxia Results in Increased IL-10 Production in a Pathogen-Independent Manner

The expression change of RORγt, BATF, and IL‐17 in Chinese vitiligo patients with 308 nanometers excimer laser treatment

Inhaled IL-10 Suppresses Lung Tumorigenesis via Abrogation of Inflammatory Macrophage–Th17 Cell Axis

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