Circulating Th1, Th2, Th9, Th17, Th22, and Treg Levels in Aortic Dissection Patients

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Abstract

Background

Previous studies demonstrated that the subsets of CD4+ T helper (Th) cells are closely related to vascular diseases, including atherosclerosis and hypertension. This study is aimed at investigating the circulating Th1, Th2, Th9, Th17, Th22, and Treg levels in aortic dissection (AD) patients.

Methods

Blood samples from AD ( n = 56) and non-AD (NAD, n = 24) patients were collected, and the circulating levels of Th1, Th2, Th9, Th17, Th22, and Treg cells and their transcription factors and functional cytokines were measured by flow cytometric analysis, quantitative polymerase chain reaction, and enzyme-linked immunosorbent assays, respectively. In addition, the human aortic vascular smooth muscle cells (HASMCs) were treated with saline, angiotensin II (Ang II), or plasma from AD patients.

Results

Compared with the levels in the NAD group, the Th1, Th9, Th17, Th22, and their transcription factor levels were increased and the Th2, Treg, and their transcription factor levels exhibited a decreasing trend in AD patients. In addition, higher IFN- γ, IL-9, IL-17, and IL-22 levels and lower IL-4 and IL-35 levels were observed in AD patients. Simple linear regression analysis and binary logistic regression analysis suggested that Th1/IFN- γ, IL-9, Th17/IL-17, and Th22/IL-22 positively regulated the occurrence of AD, while Th2/IL-4 and Treg/IL-35 negatively regulated the occurrence of AD. Plasma from AD patients further increased Bax mRNA levels but decreased Bcl2 and α-SMA mRNA levels in Ang II-treated HASMCs.

Conclusions

Changes in Th1, Th2, Th9, Th17, Th22, and Treg activity are associated with the onset of AD. Different subsets of CD4+ T cells play different roles in the presence of AD.

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Most cited references 39

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The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease.

P. Hagan, C. A. Nienaber, E. Isselbacher … (2000)

Acute aortic dissection is a life-threatening medical emergency associated with high rates of morbidity and mortality. Data are limited regarding the effect of recent imaging and therapeutic advances on patient care and outcomes in this setting. To assess the presentation, management, and outcomes of acute aortic dissection. Case series with patients enrolled between January 1996 and December 1998. Data were collected at presentation and by physician review of hospital records. The International Registry of Acute Aortic Dissection, consisting of 12 international referral centers. A total of 464 patients (mean age, 63 years; 65.3% male), 62.3% of whom had type A dissection. Presenting history, physical findings, management, and mortality, as assessed by history and physician review of hospital records. While sudden onset of severe sharp pain was the single most common presenting complaint, the clinical presentation was diverse. Classic physical findings such as aortic regurgitation and pulse deficit were noted in only 31.6% and 15.1% of patients, respectively, and initial chest radiograph and electrocardiogram were frequently not helpful (no abnormalities were noted in 12.4% and 31.3% of patients, respectively). Computed tomography was the initial imaging modality used in 61.1%. Overall in-hospital mortality was 27.4%. Mortality of patients with type A dissection managed surgically was 26%; among those not receiving surgery (typically because of advanced age and comorbidity), mortality was 58%. Mortality of patients with type B dissection treated medically was 10.7%. Surgery was performed in 20% of patients with type B dissection; mortality in this group was 31.4%. Acute aortic dissection presents with a wide range of manifestations, and classic findings are often absent. A high clinical index of suspicion is necessary. Despite recent advances, in-hospital mortality rates remain high. Our data support the need for continued improvement in prevention, diagnosis, and management of acute aortic dissection.

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The Balance of Th17 versus Treg Cells in Autoimmunity

Gap Ryol Lee (2018)

T helper type 17 (Th17) cells and pTreg cells, which share a common precursor cell (the naïve CD4 T cell), require a common tumor growth factor (TGF)-β signal for initial differentiation. However, terminally differentiated cells fulfill opposite functions: Th17 cells cause autoimmunity and inflammation, whereas Treg cells inhibit these phenomena and maintain immune homeostasis. Thus, unraveling the mechanisms that affect the Th17/Treg cell balance is critical if we are to better understand autoimmunity and tolerance. Recent studies have identified many factors that influence this balance; these factors range from signaling pathways triggered by T cell receptors, costimulatory receptors, and cytokines, to various metabolic pathways and the intestinal microbiota. This review article summarizes recent advances in our understanding of the Th17/Treg balance and its implications with respect to autoimmune disease.

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Interleukin 17 promotes angiotensin II-induced hypertension and vascular dysfunction.

Meena S Madhur, Heinrich E. Lob, Louise A. McCann … (2010)

We have shown previously that T cells are required for the full development of angiotensin II-induced hypertension. However, the specific subsets of T cells that are important in this process are unknown. T helper 17 cells represent a novel subset that produces the proinflammatory cytokine interleukin 17 (IL-17). We found that angiotensin II infusion increased IL-17 production from T cells and IL-17 protein in the aortic media. To determine the effect of IL-17 on blood pressure and vascular function, we studied IL-17(-/-) mice. The initial hypertensive response to angiotensin II infusion was similar in IL-17(-/-) and C57BL/6J mice. However, hypertension was not sustained in IL-17(-/-) mice, reaching levels 30-mm Hg lower than in wild-type mice by 4 weeks of angiotensin II infusion. Vessels from IL-17(-/-) mice displayed preserved vascular function, decreased superoxide production, and reduced T-cell infiltration in response to angiotensin II. Gene array analysis of cultured human aortic smooth muscle cells revealed that IL-17, in conjunction with tumor necrosis factor-alpha, modulated expression of >30 genes, including a number of inflammatory cytokines/chemokines. Examination of IL-17 in diabetic humans showed that serum levels of this cytokine were significantly increased in those with hypertension compared with normotensive subjects. We conclude that IL-17 is critical for the maintenance of angiotensin II-induced hypertension and vascular dysfunction and might be a therapeutic target for this widespread disease.

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Author and article information

Contributors

Jun Wan:

ORCID: http://orcid.org/0000-0003-4865-783X

Yingzhong Lin:

ORCID: http://orcid.org/0000-0003-4424-0340

Journal

Journal ID (nlm-ta): Mediators Inflamm

Journal ID (iso-abbrev): Mediators Inflamm

Journal ID (publisher-id): MI

Title: Mediators of Inflammation

Publisher: Hindawi

ISSN (Print): 0962-9351

ISSN (Electronic): 1466-1861

Publication date Collection: 2018

Publication date (Electronic): 6 September 2018

Volume: 2018

Electronic Location Identifier: 5697149

Affiliations

¹Department of Cardiology, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, China

²Department of Cardiology, Hubei Key Laboratory of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute, Wuhan University, Wuhan 430060, China

³Emergency & Critical Care Center, Beijing Institute of Heart, Lung, and Blood Vessel Diseases, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China

⁴Department of Ultrasound, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning 530021, China

⁵Department of Cardiology, Handan First Hospital, Handan 056002, China

Author notes

Academic Editor: Elena Dozio

Author information

Jun Wan http://orcid.org/0000-0003-4865-783X

Yingzhong Lin http://orcid.org/0000-0003-4424-0340

Article

DOI: 10.1155/2018/5697149

PMC ID: 6146596

SO-VID: d99c86b4-c842-4e89-90de-be913f5d89c8

License:

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date received : 24 March 2018

Date revision received : 21 June 2018

Date accepted : 26 July 2018

Funding

Funded by: National Natural Science Foundation of China

Award ID: 81770472

Award ID: 81460081

Award ID: 81460061

Award ID: 81760051

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Circulating Th1, Th2, Th9, Th17, Th22, and Treg Levels in Aortic Dissection Patients

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Abstract

Background

Methods

Results

Conclusions

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Regulatory T cell (Treg) therapy

Most cited references 39

The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease.

The Balance of Th17 versus Treg Cells in Autoimmunity

Interleukin 17 promotes angiotensin II-induced hypertension and vascular dysfunction.

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Cited by 31

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