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Article ; Online: Interleukin 17 in vascular inflammation.

von Vietinghoff, Sibylle / Ley, Klaus

2010 Volume 21, Issue 6, Page(s) 463–469

Abstract: ... vascular inflammation, both in chronic forms such as atherosclerosis and in acute vasculitis. IL-17 has ... Interleukin (IL)-17 (also known as IL-17A) is produced by activated T cells. It is a marker ... In acute inflammation, IL-17 is elevated and may be causally involved in the autoimmune vasculitides ...

Abstract	Interleukin (IL)-17 (also known as IL-17A) is produced by activated T cells. It is a marker cytokine of the T(H₁₇) lineage. IL-17 production is induced in infections, autoimmune diseases and other inflammatory events. IL-17 is involved in host defense, but also inflammatory tissue destruction. Vascular disease, mostly in the chronic form of atherosclerosis, is a leading cause of death. While normal vessels harbor only few leukocytes, large numbers of both innate and adaptive immune cells accumulate during vascular inflammation, both in chronic forms such as atherosclerosis and in acute vasculitis. IL-17 has a role in chronic vascular inflammation of atherosclerosis and possibly hypertensive vascular changes. In acute inflammation, IL-17 is elevated and may be causally involved in the autoimmune vasculitides including vasculitis in systemic lupus erythematodes. Blood vessels are important targets in alloimmune graft rejection and a number of studies provide data on a role of IL-17 in this context. This brief review summarizes the currently available evidence for and putative mechanisms of action of IL-17 in mouse models of and human vascular disease.
MeSH term(s)	Acute Coronary Syndrome/immunology ; Animals ; Apolipoproteins E/deficiency ; Atherosclerosis/immunology ; Autoimmune Diseases/immunology ; Humans ; Hypertension/pathology ; Interleukin-17/biosynthesis ; Interleukin-17/immunology ; Leukocytes/physiology ; Lupus Erythematosus, Systemic/immunology ; Mice ; Vasculitis/immunology
Chemical Substances	Apolipoproteins E ; Interleukin-17
Language	English
Publishing date	2010-11-12
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1330534-7
ISSN	1879-0305 ; 1359-6101
ISSN (online)	1879-0305
ISSN	1359-6101
DOI	10.1016/j.cytogfr.2010.10.003
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Article ; Online: Interleukin 17 drives vascular inflammation, endothelial dysfunction, and arterial hypertension in psoriasis-like skin disease.

Karbach, Susanne / Croxford, Andrew L / Oelze, Matthias / Schüler, Rebecca / Minwegen, Daniel / Wegner, Joanna / Koukes, Lija / Yogev, Nir / Nikolaev, Alexei / Reißig, Sonja / Ullmann, Alexander / Knorr, Maike / Waldner, Maximilian / Neurath, Markus F / Li, Huige / Wu, Zhixiong / Brochhausen, Christoph / Scheller, Jürgen / Rose-John, Stefan /

Piotrowski, Carolin / Bechmann, Ingo / Radsak, Markus / Wild, Philipp / Daiber, Andreas / von Stebut, Esther / Wenzel, Philip / Waisman, Ari / Münzel, Thomas

Arteriosclerosis, thrombosis, and vascular biology

2014 Volume 34, Issue 12, Page(s) 2658–2668

Abstract: ... that overproduction of IL-17A in the skin leading to dermal inflammation may systemically cause vascular dysfunction ... increased vascular production of the nitric oxide/superoxide reaction product peroxynitrite and infiltration ... Dermal overexpression of IL-17A induces systemic endothelial dysfunction, vascular oxidative stress ...

Abstract	Objective: Interleukin (IL)-17A is regarded as an important cytokine to drive psoriasis, an inflammatory skin disease marked by increased cardiovascular mortality. We aimed to test the hypothesis that overproduction of IL-17A in the skin leading to dermal inflammation may systemically cause vascular dysfunction in psoriasis-like skin disease. Approach and results: Conditional overexpression of IL-17A in keratinocytes caused severe psoriasis-like skin inflammation in mice (K14-IL-17A(ind/+) mice), associated with increased reactive oxygen species formation and circulating CD11b(+) inflammatory leukocytes in blood, with endothelial dysfunction, increased systolic blood pressure, left ventricular hypertrophy, and reduced survival compared with controls. In K14-IL-17A(ind/+) mice, immunohistochemistry and flow cytometry revealed increased vascular production of the nitric oxide/superoxide reaction product peroxynitrite and infiltration of the vasculature with myeloperoxidase(+)CD11b(+)GR1(+)F4/80(-) cells accompanied by increased expression of the inducible nitric oxide synthase and the nicotinamide dinucleotide phosphate (NADPH) oxidase, nox2. Neutrophil depletion by anti-GR-1 antibody injections reduced oxidative stress in blood and vessels. Neutralization of tumor necrosis factor-α and IL-6 (both downstream of IL-17A) reduced skin lesions, attenuated oxidative stress in heart and blood, and partially improved endothelial dysfunction in K14-IL-17A(ind/+) mice. Conclusions: Dermal overexpression of IL-17A induces systemic endothelial dysfunction, vascular oxidative stress, arterial hypertension, and increases mortality mainly driven by myeloperoxidase(+)CD11b(+)GR1(+)F4/80(-) inflammatory cells. Depletion of the GR-1(+) immune cells or neutralization of IL-17A downstream cytokines by biologicals attenuates the vascular phenotype in K14-IL-17A(ind/+) mice.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Animals ; Aorta/pathology ; Cardiovascular Diseases/etiology ; Case-Control Studies ; Disease Models, Animal ; Endothelium, Vascular/immunology ; Endothelium, Vascular/physiopathology ; Female ; Humans ; Hypertension/etiology ; Hypertension/immunology ; Hypertension/physiopathology ; Interleukin-17/genetics ; Interleukin-17/physiology ; Interleukin-6/antagonists & inhibitors ; Interleukin-6/physiology ; Keratinocytes/immunology ; Keratinocytes/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Middle Aged ; Myocytes, Cardiac/pathology ; Neutrophils/pathology ; Neutrophils/physiology ; Nitric Oxide/metabolism ; Psoriasis/complications ; Psoriasis/etiology ; Psoriasis/physiopathology ; Reactive Oxygen Species/metabolism ; Risk Factors ; Tumor Necrosis Factor-alpha/antagonists & inhibitors ; Tumor Necrosis Factor-alpha/physiology ; Up-Regulation ; Vasculitis/etiology ; Vasculitis/immunology ; Vasculitis/physiopathology
Chemical Substances	IL17A protein, human ; Il17a protein, mouse ; Interleukin-17 ; Interleukin-6 ; Reactive Oxygen Species ; Tumor Necrosis Factor-alpha ; Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	2014-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.114.304108
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Article ; Online: Interleukin-17 (IL-17) triggers systemic inflammation, peripheral vascular dysfunction, and related prothrombotic state in a mouse model of Alzheimer's disease.

Vellecco, Valentina / Saviano, Anella / Raucci, Federica / Casillo, Gian Marco / Mansour, Adel Abo / Panza, Elisabetta / Mitidieri, Emma / Femminella, Grazia Daniela / Ferrara, Nicola / Cirino, Giuseppe / Sorrentino, Raffaella / Iqbal, Asif Jilani / d'Emmanuele di Villa Bianca, Roberta / Bucci, Mariarosaria / Maione, Francesco

Pharmacological research

2022 Volume 187, Page(s) 106595

Abstract: ... amyloid-β-induced neuro-inflammation and memory impairment, demonstrating the pivotal role of IL-17 in AD ... vascular networks and platelet function. However, not much is known about peripheral vascular inflammation ... such as systemic inflammation, peripheral vascular dysfunction, and related pro-thrombotic state in a non-genetic ...

Abstract	Alzheimer's disease (AD) is one of the most prevalent forms of neurodegenerative disorders. Previously, we have shown that in vivo administration of an IL-17 neutralizing antibody (IL-17Ab) rescues amyloid-β-induced neuro-inflammation and memory impairment, demonstrating the pivotal role of IL-17 in AD-derived cognitive deficit. Recently, AD has been recognized as a more intriguing pathology affecting vascular networks and platelet function. However, not much is known about peripheral vascular inflammation and how pro-inflammatory circulating cells/mediators could affect peripheral vessels' function. This study aimed to evaluate whether IL-17Ab treatment could also impact peripheral AD features, such as systemic inflammation, peripheral vascular dysfunction, and related pro-thrombotic state in a non-genetic mouse model of AD. Mice were injected intracerebroventricularly with Aβ
MeSH term(s)	Animals ; Mice ; Alzheimer Disease/drug therapy ; Alzheimer Disease/pathology ; Amyloid beta-Peptides ; Cytokines ; Disease Models, Animal ; Inflammation/drug therapy ; Inflammation/pathology ; Interleukin-17 ; Peptide Fragments/pharmacology
Chemical Substances	Amyloid beta-Peptides ; Cytokines ; Interleukin-17 ; Peptide Fragments ; Il17a protein, mouse
Language	English
Publishing date	2022-12-05
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1003347-6
ISSN	1096-1186 ; 0031-6989 ; 1043-6618
ISSN (online)	1096-1186
ISSN	0031-6989 ; 1043-6618
DOI	10.1016/j.phrs.2022.106595
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Zs.A 721: Show issues

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Article ; Online: Targeting interleukin-17 in radiation-induced toxicity and cancer progression.

Baindara, Piyush

Cytokine & growth factor reviews

2024 Volume 75, Page(s) 31–39

Abstract: ... IL-6, TNF-α, and TGF-β, also cause the production of Interleukin-17 (IL-17), a cytokine that is ... by radiation therapy. However, currently, the role of IL-17 in RT-induced toxicity in conjunction with cancer ... from the literature implicating IL-17 in radiation-mediated tissue injuries and the efficacy of tRT in lung cancer ...

Abstract	Recent strategies to combine chemoradiation with immunotherapy to treat locally advanced lung cancer have improved five-year survival outcomes. However, collateral toxicity to healthy lungs, esophagus, cardiac, and vascular tissue continues to limit the effectiveness of curative-intent thoracic radiation (tRT). It is necessary to gain a deeper comprehension of the fundamental mechanisms underlying inflammation-mediated radiation-induced damage to normal cells. Several cells have been linked in published studies to the release of cytokines and chemokines after radiation therapy. Several inflammatory mediators, such as IL-1, IL-6, TNF-α, and TGF-β, also cause the production of Interleukin-17 (IL-17), a cytokine that is essential for maintaining immunological homeostasis and plays a role in the toxicity caused by radiation therapy. However, currently, the role of IL-17 in RT-induced toxicity in conjunction with cancer progression remains poorly understood. This review provides an overview of the most recent data from the literature implicating IL-17 in radiation-mediated tissue injuries and the efficacy of tRT in lung cancer, as well as its potential as a therapeutic target for interventions to reduce the side effects of tRT with curative intent and to boost an anti-tumor immune response to improve treatment outcomes. IL-17 may also act as a biomarker for predicting the effectiveness of a given treatment as well as the toxicity caused by tRT.
MeSH term(s)	Humans ; Interleukin-17 ; Cytokines ; Lung/pathology ; Lung Neoplasms/radiotherapy ; Radiation Injuries/therapy ; Radiation Injuries/pathology
Chemical Substances	Interleukin-17 ; Cytokines
Language	English
Publishing date	2024-01-05
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1330534-7
ISSN	1879-0305 ; 1359-6101
ISSN (online)	1879-0305
ISSN	1359-6101
DOI	10.1016/j.cytogfr.2024.01.001
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Article ; Online: Aggravated Atherosclerosis and Vascular Inflammation With Reduced Kidney Function Depend on Interleukin-17 Receptor A and Are Normalized by Inhibition of Interleukin-17A.

Nordlohne, Johannes / Helmke, Alexandra / Ge, Shuwang / Rong, Song / Chen, Rongjun / Waisman, Ari / Haller, Hermann / von Vietinghoff, Sibylle

JACC. Basic to translational science

2018 Volume 3, Issue 1, Page(s) 54–66

Abstract: ... show, in a mouse model of atherosclerosis in moderate renal impairment, that interleukin-17 receptor ... studies have reported enhanced vascular inflammation in mice and recently also in humans. Our current data ... A is instrumental in this condition, and blockade of this pathway can normalize arterial inflammation ...

Abstract	Effective therapy of atherosclerotic complications in patients with chronic kidney disease (CKD) is an unmet clinical need. Cardiovascular events are the most common cause of death. At a glomerular filtration rate ≤60 ml/min, these events are increased also after correction for common risk factors. Previous studies have reported enhanced vascular inflammation in mice and recently also in humans. Our current data show, in a mouse model of atherosclerosis in moderate renal impairment, that interleukin-17 receptor A is instrumental in this condition, and blockade of this pathway can normalize arterial inflammation even in advanced atherosclerosis.
Language	English
Publishing date	2018-01-10
Publishing country	United States
Document type	Journal Article
ISSN	2452-302X
ISSN (online)	2452-302X
DOI	10.1016/j.jacbts.2017.08.005
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Article ; Online: CD1d-Dependent Natural Killer T Cells Mediate Hypertension and Vascular Injury Through Interleukin-17A.

Xiao, Xue / Hou, Cui-Liu / Zhang, Yun-Long / Yang, Hui / Wang, Xiao-Xiao / Wang, Hong-Xia

Journal of the American Heart Association

2023 Volume 12, Issue 13, Page(s) e029179

Abstract: ... interleukin-17A partially reversed Ang II-induced hypertension and vascular injury in CD1dko mice. In addition ... vascular injury. Methods and Results Hypertension models were induced in male CD1d knockout (CD1dko), wild-type ... Blood pressure was measured by the tail-cuff system and radiotelemetry. Vascular injury was assessed ...

Abstract	Background Different T-lymphocyte subsets, including CD1d-dependent natural killer T (NKT) cells, play distinct roles in hypertension, highlighting the importance of identifying key immune cells for its treatment. This study aimed to determine the unknown effects of CD1d-dependent NKT cells on hypertension and vascular injury. Methods and Results Hypertension models were induced in male CD1d knockout (CD1dko), wild-type, and adoptive bone marrow transfer mice by angiotensin II (Ang II) or deoxycorticosterone acetate salt. Blood pressure was measured by the tail-cuff system and radiotelemetry. Vascular injury was assessed by histologic studies or aortic ring assay. Inflammation was detected by flow cytometry, quantitative real-time polymerase chain reaction, or ELISA. Results showed that Ang II infusion significantly reduced CD1d expression and NKT cell numbers in the aorta of mice. CD1dko mice exhibited worsened blood pressure elevation, vascular injury, and inflammatory response induced by Ang II or deoxycorticosterone acetate salt. However, these effects were markedly reversed in wild-type mice treated with NKT cell-specific activator. Adoptive transfer of CD1dko bone marrow cells to wild-type mice also significantly worsened Ang II-induced responses. Mechanistically, CD1dko increased Ang II-induced interleukin-6 production and activated signal transducer and activator of transcription 3 and orphan nuclear receptor γ, subsequently inducing interleukin-17A production. Neutralizing interleukin-17A partially reversed Ang II-induced hypertension and vascular injury in CD1dko mice. In addition, levels of NKT cells were lower in the blood of patients with hypertension (n=57) compared with normotensive individuals (n=87). Conclusions These findings reveal a previously unknown role for CD1d-dependent NKT cells in hypertension and vascular injury, indicating that NKT cell activation could be a promising therapeutic target for hypertension.
MeSH term(s)	Animals ; Male ; Mice ; Acetates/adverse effects ; Acetates/metabolism ; Desoxycorticosterone/adverse effects ; Desoxycorticosterone/metabolism ; Hypertension/chemically induced ; Hypertension/metabolism ; Interleukin-17/metabolism ; Mice, Inbred C57BL ; Mice, Knockout ; Natural Killer T-Cells/metabolism ; Vascular System Injuries/metabolism
Chemical Substances	Acetates ; Desoxycorticosterone (40GP35YQ49) ; Interleukin-17 ; Il17a protein, mouse ; CD1d antigen, mouse
Language	English
Publishing date	2023-06-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2653953-6
ISSN	2047-9980 ; 2047-9980
ISSN (online)	2047-9980
ISSN	2047-9980
DOI	10.1161/JAHA.122.029179
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Article ; Online: Interleukin-17-targeted treatment in patients with spondyloarthritis and associated cardiometabolic risk profile.

Queiro, Rubén / Aurrecoechea, Elena / Alonso Castro, Sara / Villa Blanco, Ignacio / Brandy-Garcia, Anahy / Linge, Raquel

Frontiers in immunology

2023 Volume 14, Page(s) 1203372

Abstract: ... of interleukin (IL)-17 blockade versus other molecular mechanisms in patients with cardiometabolic conditions ... inflammation and tissue remodeling at the affected joints and entheses. The importance of the IL-23/IL-17 ... The IL-23/IL-17 axis plays a pivotal role in the pathophysiology of spondyloarthritis by promoting ...

Abstract	Spondyloarthritis is a group of immune-mediated rheumatic disorders that significantly impact patients' physical function and quality of life. Patients with spondyloarthritis experience a greater prevalence of cardiometabolic disorders, such as obesity, hypertension, dyslipidemia and diabetes mellitus, and these comorbidities are associated with increased spondyloarthritis disease activity and risk of cardiovascular events. This narrative review summarizes the evidence for a physiological link between inflammatory status and cardiometabolic comorbidities in spondyloarthritis, as well as the impact of interleukin (IL)-17 blockade versus other molecular mechanisms in patients with cardiometabolic conditions. The IL-23/IL-17 axis plays a pivotal role in the pathophysiology of spondyloarthritis by promoting inflammation and tissue remodeling at the affected joints and entheses. The importance of the IL-23/IL-17 signaling cascade in underlying sub-clinical inflammation in common cardiometabolic disorders suggests the existence of shared pathways between these processes and spondyloarthritis pathophysiology. Thus, a bidirectional relationship exists between the effects of biologic drugs and patients' cardiometabolic profile, which must be considered during treatment decision making. Biologic therapy may induce changes in patients' cardiometabolic status and cardiometabolic conditions may conversely impact the clinical response to biologic therapy. Available evidence regarding the impact of IL-17 blockade with secukinumab on cardiometabolic parameters suggests this drug does not interfere with traditional cardiovascular risk markers and could be associated with a decreased risk of cardiovascular events. Additionally, the efficacy and retention rates of secukinumab do not appear to be negatively affected by obesity, with some studies reporting a positive impact on clinical outcomes, contrary to that described with other approaches, such as tumor necrosis factor blockade. In this article, we also review evidence for this bidirectional association with other treatments for spondyloarthritis. Current evidence suggests that IL-17-targeted therapy with secukinumab is highly effective in spondyloarthritis patients with cardiometabolic comorbidities and may provide additional cardiometabolic benefits.
MeSH term(s)	Humans ; Antibodies, Monoclonal/therapeutic use ; Interleukin-17 ; Quality of Life ; Spondylarthritis/drug therapy ; Inflammation/drug therapy ; Interleukin-23 ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/drug therapy
Chemical Substances	Antibodies, Monoclonal ; Interleukin-17 ; Interleukin-23
Language	English
Publishing date	2023-07-18
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1203372
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Article ; Online: C-Reactive Protein, Interleukin-6, and Vascular Recurrence After Stroke: An Individual Participant Data Meta-Analysis.

McCabe, John J / Walsh, Cathal / Gorey, Sarah / Harris, Katie / Hervella, Pablo / Iglesias-Rey, Ramon / Jern, Christina / Li, Linxin / Miyamoto, Nobukazu / Montaner, Joan / Pedersen, Annie / Purroy, Francisco / Rothwell, Peter M / Sudlow, Catherine / Ueno, Yuji / Vicente-Pascual, Mikel / Whiteley, William / Woodward, Mark / Kelly, Peter J

Stroke

2023 Volume 54, Issue 5, Page(s) 1289–1299

Abstract: ... markers of inflammation were independently associated with vascular recurrence after stroke, strengthening ... 1407 (16.7% [95% CI, 15.9-17.5]) patients had MACE and 1191 (14.1% [95% CI, 13.4-14.9]) patients had ... Background: Anti-inflammatory therapies reduce recurrent vascular events in coronary disease ...

Abstract	Background: Anti-inflammatory therapies reduce recurrent vascular events in coronary disease. Existing studies have reported highly conflicting findings for the association of blood inflammatory markers with vascular recurrence after stroke leading to uncertainty about the potential of anti-inflammatory therapies after stroke and no consensus about the utility of measurement of inflammatory markers in current guidelines. Methods: We investigated the association between hsCRP (high-sensitivity C-reactive protein), IL-6 (interluekin-6), and recurrent major adverse cardiovascular events (MACE), and stroke from individual participant data from 8420 patients with ischemic stroke/transient ischemic attack from 10 prospective studies. We did within-study multivariable regression analyses and then combined adjusted risk ratio (RR) by random-effects meta-analysis. Results: During 18 920 person-years of follow-up, 1407 (16.7% [95% CI, 15.9-17.5]) patients had MACE and 1191 (14.1% [95% CI, 13.4-14.9]) patients had recurrent stroke. On bivariate analysis, baseline IL-6 was associated with MACE (RR, 1.26 [95% CI, 1.10-1.43]) and recurrent stroke (RR, 1.18 [95% CI, 1.05-1.32]), per unit increase log Conclusions: Blood markers of inflammation were independently associated with vascular recurrence after stroke, strengthening the rationale for randomized trials of anti-inflammatory therapies for secondary prevention after ischemic stroke/TIA.
MeSH term(s)	Humans ; Interleukin-6 ; C-Reactive Protein/analysis ; Ischemic Attack, Transient/prevention & control ; Prospective Studies ; Stroke/prevention & control ; Ischemic Stroke ; Recurrence
Chemical Substances	Interleukin-6 ; C-Reactive Protein (9007-41-4)
Language	English
Publishing date	2023-04-07
Publishing country	United States
Document type	Meta-Analysis ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80381-9
ISSN	1524-4628 ; 0039-2499 ; 0749-7954
ISSN (online)	1524-4628
ISSN	0039-2499 ; 0749-7954
DOI	10.1161/STROKEAHA.122.040529
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Zs.A 448: Show issues

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Article ; Online: Interleukin-17 deficiency reduced vascular inflammation and development of atherosclerosis in Western diet-induced apoE-deficient mice.

Usui, Fumitake / Kimura, Hiroaki / Ohshiro, Taichi / Tatsumi, Kazuki / Kawashima, Akira / Nishiyama, Akiyo / Iwakura, Yo-Ichiro / Ishibashi, Shun / Takahashi, Masafumi

Biochemical and biophysical research communications

2012 Volume 420, Issue 1, Page(s) 72–77

Abstract: ... Our results indicate that IL-17 deficiency reduces vascular inflammation and atherosclerosis and ... in WD-fed apoE(-/-)IL-17(-/-) mice compared with WD-fed apoE(-/-) mice, whereas vascular ... Objective: Several reports describe the role of interleukin (IL)-17 in the development ...

Abstract	Objective: Several reports describe the role of interleukin (IL)-17 in the development of atherosclerosis; however, its precise role remains controversial. We generated double-deficient mice for apolipoprotein E (apoE) and IL-17 (apoE(-/-)IL-17(-/-) mice) and investigated the effect of IL-17 deficiency on vascular inflammation and atherosclerosis. Methods and results: Atherosclerotic plaque areas in apoE(-/-)IL-17(-/-) mice fed a Western diet (WD) were significantly reduced compared with those in apoE(-/-) mice. No significant differences in plasma lipid profiles were observed between apoE(-/-) and apoE(-/-)IL-17(-/-) mice. The number of infiltrated macrophages in the plaques was significantly decreased in WD-fed apoE(-/-)IL-17(-/-) mice compared with WD-fed apoE(-/-) mice, whereas vascular smooth muscle cell content was not altered by IL-17 deficiency. Expression of inflammatory cytokines (MCP-1, IL-1β, IL-6, IFN-γ, and IL-12 p40) and scavenger receptors (Msr-1, Scarb1, and Olr1) in the plaques was inhibited in WD-fed apoE(-/-)IL-17(-/-) mice. Furthermore, expression of inducible nitric oxide (M1 marker) and arginase-1 (M2 marker) was inhibited in WD-fed apoE(-/-)IL-17(-/-) mice. Conclusion: Our results indicate that IL-17 deficiency reduces vascular inflammation and atherosclerosis and that modulation of IL-17 could be a potential target for prevention and treatment of atherosclerosis.
MeSH term(s)	Animals ; Apolipoproteins E/genetics ; Atherosclerosis/genetics ; Atherosclerosis/immunology ; Cytokines/biosynthesis ; Diet/adverse effects ; Disease Models, Animal ; Interleukin-17/genetics ; Macrophages/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Vasculitis/genetics ; Vasculitis/immunology
Chemical Substances	Apolipoproteins E ; Cytokines ; Interleukin-17
Language	English
Publishing date	2012-03-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2012.02.117
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Article ; Online: Drug-induced entero-colitis due to interleukin-17 inhibitor use; capsule endoscopic findings and pathological characteristics: A case report.

Saito, Keita / Yoza, Kiichiro / Takeda, Shinichiro / Shimoyama, Yoshihiro / Takeuchi, Ken

World journal of gastroenterology

2023 Volume 29, Issue 32, Page(s) 4912–4919

Abstract: Background: Interleukin-17 (IL-17) inhibitors are known to cause exacerbation or new onset ... scarring of the colon were endoscopically confirmed.: Conclusion: To the best of our knowledge, 17 ... reports have documented IL-17 inhibitor-induced entero-colitis with endoscopic images, endoscopic findings ...

Abstract	Background: Interleukin-17 (IL-17) inhibitors are known to cause exacerbation or new onset of inflammatory bowel disease upon administration. However, few reports have described characteristic endoscopic and histopathologic findings, and no small intestinal lesions have been reported so far. Case summary: A woman in her 60s with psoriasis was administered ixekizumab (IXE), an anti-IL-17A antibody, for the treatment of psoriasis. Twenty months after commencing treatment, the patient visited our hospital because of persistent diarrhea. Blood tests performed at the time of the visit revealed severe inflammation, and colonoscopy revealed multiple round ulcers throughout the colon. A tissue biopsy of the ulcer revealed infiltration of inflammatory cells and granuloma-like findings in the submucosal layer. Capsule endoscopy revealed multiple jejunal erosions. After the withdrawal of IXE, the symptoms gradually improved, and ulcer reduction and scarring of the colon were endoscopically confirmed. Conclusion: To the best of our knowledge, 17 reports have documented IL-17 inhibitor-induced entero-colitis with endoscopic images, endoscopic findings, and pathological characteristics, including the present case. Nine of these cases showed diffuse loss of vascular pattern, coarse mucosa/ulcer formation in the left colon, and endoscopic findings similar to those of ulcerative colitis. In the remaining eight cases, discontinuous erosions and ulcerations from the terminal ileum to the rectum were seen, with endoscopic findings similar to those of Crohn's disease. In this case, the findings were confirmed by capsule endoscopy, which has not been previously reported.
MeSH term(s)	Humans ; Female ; Capsule Endoscopy ; Interleukin-17 ; Ulcer/chemically induced ; Capsule Endoscopes ; Colitis/chemically induced ; Colitis/drug therapy
Chemical Substances	Interleukin-17
Language	English
Publishing date	2023-08-29
Publishing country	United States
Document type	Case Reports
ZDB-ID	2185929-2
ISSN	2219-2840 ; 1007-9327
ISSN (online)	2219-2840
ISSN	1007-9327
DOI	10.3748/wjg.v29.i32.4912
Database	MEDical Literature Analysis and Retrieval System OnLINE

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