IL-17RA Is Required for CCL2 Expression, Macrophage Recruitment, and Emphysema in Response to Cigarette Smoke

Chen, Kong; Pociask, Derek; McAleer, Jeremy P.; Chan, Yvonne R.; Alcorn, John F.; Kreindler, James L.; Keyser, Matthew R.; Shapiro, Steven D.; Houghton, A. McGarry; Kolls, Jay K.; Zheng, Mingquan

doi:10.1371/journal.pone.0020333

Cited by 146 publications

(147 citation statements)

References 37 publications

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“…It is therefore conceivable that IL-22 production is promoted by direct effects on T-cells of AHR agonists present in cigarette smoke. This is supported by recent findings in the mouse [34] and in humans [35], demonstrating that addition of cigarette smoke extract to T-cells undergoing Th17 differentiation augments the percentage of IL-22 producing cells via an AHR-dependent mechanism. Future studies should also examine a group of smokers with normal lung function to see if these results can be confirmed in this control group.…”

Section: Effects Of Smoking On Cytokine Expressionsupporting

confidence: 77%

Systemic CD4+ and CD8+ T-cell cytokine profiles correlate with GOLD stage in stable COPD

et al. 2011

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Chronic obstructive pulmonary disease (COPD) is associated with pulmonary and systemic inflammation. Both CD4+ and CD8+ T-lymphocytes play a key role in COPD pathogenesis, but cytokine profiles in circulating T-lymphocytes have not been well characterised.Here we report the analysis of peripheral blood T-cells from 30 stable COPD patients and 10 healthy never-smokers for interferon (IFN)-c, interleukin (IL)-4, tumour necrosis factor (TNF)-a and the T-helper 17 cytokines IL-17A, IL-17F and IL-22 by intracellular flow cytometry.We found significantly increased proportions of IFN-c+ and TNF-a+ CD8+ T-cells in COPD patients, when compared with healthy controls. This was most evident in patients with less severe disease. In contrast, expression profiles in circulating CD4+ T-cells were similar in COPD patients and healthy controls for all cytokines tested, except for IL-17F. COPD patients with more severely reduced diffusing capacity had lower proportions of IL-17A+ CD4+ T-cells. Proportions of IL-22+ cells in the CD4+ memory T-cell population were significantly increased in active smokers, when compared with past smokers.Collectively, this comprehensive cytokine analysis of circulating T-cells in COPD patients revealed a correlation for CD8+ T-cells between Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage and IFN-c or TNF-a expression, but not for CD4+ T-cells.

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Section: Effects Of Smoking On Cytokine Expressionsupporting

confidence: 77%

Systemic CD4+ and CD8+ T-cell cytokine profiles correlate with GOLD stage in stable COPD

et al. 2011

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“…More recent reports unraveled beneficial effects of SFN in experimental chronic obstructive pulmonary disease (COPD) (28,53). SFN reduced pulmonary inflammation in COPD, a condition associated with Th17 responses (54,55). The aim of our study was to elucidate the immunoregulatory capabilities of SFN in terms of affected immune cells and underlying molecular mechanisms during T cell-mediated autoimmune responses.…”

Section: Sfn Treatment Inhibits Il23a/il12b Expression and Th17/th1 Dmentioning

confidence: 99%

Sulforaphane Protects from T Cell–Mediated Autoimmune Disease by Inhibition of IL-23 and IL-12 in Dendritic Cells

Geisel

Brück

Glocova

et al. 2014

The Journal of Immunology

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Sulforaphane (SFN), an isothiocyanate, is part of an important group of naturally occurring small molecules with anti-inflammatory properties. The published reports are best conceivable with an inhibition of T cell function, but the mode of action remains unknown. We therefore analyzed the effect of SFN on T cell–mediated autoimmune disease. Feeding mice with SFN protected from severe experimental autoimmune encephalomyelitis. Disease amelioration was associated with reduced IL-17 and IFN-γ expression in draining lymph nodes. In vitro, SFN treatment of T cells did not directly alter T cell cytokine secretion. In contrast, SFN treatment of dendritic cells (DCs) inhibited TLR4-induced IL-12 and IL-23 production, and severely suppressed Th1 and Th17 development of T cells primed by SFN-treated DCs. SFN regulated the activity of the TLR4-induced transcription factor NF-κB, without affecting the degradation of its inhibitor IκB-α. Instead, SFN treatment of DCs resulted in strong expression of the stress response protein heme oxygenase-1 (HO-1), which interacts with and thereby inhibits NF-κB p65. Consistent with these findings, HO-1 bound to p65 and subsequently inhibited the p65 activity at the IL23a and IL12b promoters. Importantly, SFN suppressed Il23a and Il12b expression in vivo and silenced Th17/Th1 responses within the CNS. Thus, our data show that SFN improves Th17/Th1-mediated autoimmune disease by inducing HO-1 and inhibiting NF-κB p65-regulated IL-23 and IL-12 expression.

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“…The effect of rhMMP-12 was also examined on human alveolar type II-like epithelial cells (A549) and on human bronchial epithelial cells (BEAS-2B), showing that rhMMP-12 enhances the release of several chemokines by A549 cells, in particular, monocyte chemoattractant protein-1 (MCP-1)/CCL2, growth-related oncogene-a (GRO-a)/CXCL1, and IL-8/CXCL8 (Le Quement et al, 2008). In their study Chen and colleagues have partially elucidated the immunological mechanisms leading to pathologic changes associated to COPD (Chen et al, 2011b). They have shown that cigarette smoke is a powerful T helper 17 [Th17] cells adjuvant and that interleukin 17A receptor signaling is required for chemokine expression necessary for MMP-12 induction and tissue emphysema (Chen et al, 2011b).…”

Section: Spinal Cord Injury (Sci)mentioning

confidence: 99%

“…In their study Chen and colleagues have partially elucidated the immunological mechanisms leading to pathologic changes associated to COPD (Chen et al, 2011b). They have shown that cigarette smoke is a powerful T helper 17 [Th17] cells adjuvant and that interleukin 17A receptor signaling is required for chemokine expression necessary for MMP-12 induction and tissue emphysema (Chen et al, 2011b).…”

Section: Spinal Cord Injury (Sci)mentioning

confidence: 99%

Human matrix metalloproteinases: An ubiquitarian class of enzymes involved in several pathological processes

Sbardella

Fasciglione

Gioia

et al. 2012

Molecular Aspects of Medicine

209

212

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a b s t r a c tHuman matrix metalloproteinases (MMPs) belong to the M10 family of the MA clan of endopeptidases. They are ubiquitarian enzymes, structurally characterized by an active site where a Zn 2+ atom, coordinated by three histidines, plays the catalytic role, assisted by a glutamic acid as a general base. Various MMPs display different domain composition, which is very important for macromolecular substrates recognition. Substrate specificity is very different among MMPs, being often associated to their cellular compartmentalization and/or cellular type where they are expressed. An extensive review of the different MMPs structural and functional features is integrated with their pathological role in several types of diseases, spanning from cancer to cardiovascular diseases and to neurodegeneration. It emerges a very complex and crucial role played by these enzymes in many physiological and pathological processes.

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IL-17RA Is Required for CCL2 Expression, Macrophage Recruitment, and Emphysema in Response to Cigarette Smoke

Cited by 146 publications

References 37 publications

Systemic CD4+ and CD8+ T-cell cytokine profiles correlate with GOLD stage in stable COPD

Systemic CD4+ and CD8+ T-cell cytokine profiles correlate with GOLD stage in stable COPD

Sulforaphane Protects from T Cell–Mediated Autoimmune Disease by Inhibition of IL-23 and IL-12 in Dendritic Cells

Human matrix metalloproteinases: An ubiquitarian class of enzymes involved in several pathological processes

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