Circulating Th1, Th2, and Th17 Levels in Hypertensive Patients

Ji, Qingwei; Cheng, Guojie; Ma, Ning; Huang, Ying; Lin, Yingzhong; Zhou, Qi; Qu, Bin; Dong, Jianzeng; Zhou, Yujie; Nie, Shaoping

doi:10.1155/2017/7146290

Cited by 60 publications

(33 citation statements)

References 29 publications

(53 reference statements)

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“…Exogenous Ang II treatment mediated a strong Th1 immune response and increased IFN-γ expression, whereas it reduced the Th2 immune response and decreased IL-4 secretion. Further, the changes in Th1/IFN-γ and Th2/IL-4 levels were related to Ang II-induced hypertension or the onset of kidney injury [25,26]. These studies suggest that imbalance in Th1 and Th2 is closely related to the progression of hypertension or hypertensive complications.…”

Section: Cd4+ T Helper (Th) Cells Include Regulatory T Cells (Treg) Amentioning

confidence: 73%

Interleukin-9 Deletion Relieves Vascular Dysfunction and Decreases Blood Pressure via the STAT3 Pathway in Angiotensin II-Treated Mice

Yang

Tang

Zhai

et al. 2020

Mediators of Inflammation

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Background. Multiple interleukin (IL) family members were reported to be closely related to hypertension. We aimed to investigate whether IL-9 affects angiotensin II- (Ang II-) induced hypertension in mice. Methods. Mice were treated with Ang II, and IL-9 expression was determined. In addition, effects of IL-9 knockout (KO) on blood pressure were observed in Ang II-infused mice. To determine whether the effects of IL-9 on blood pressure was mediated by the signal transducer and activator of the transcription 3 (STAT3) pathway, Ang II-treated mice were given S31-201. Furthermore, circulating IL-9 levels in patients with hypertension were measured. Results. Ang II treatment increased serum and aortic IL-9 expression in a dose-dependent manner; IL-9 levels were the highest in the second week and continued to remain high into the fourth week after the treatment. IL-9 KO downregulated proinflammatory cytokine expression, whereas it upregulated anti-inflammatory cytokine levels, relieved vascular dysfunction, and decreased blood pressure in Ang II-infused mice. IL-9 also reduced smooth muscle 22α (SM22α) expression and increased osteopontin (OPN) levels both in mice and in vitro. The effects of IL-9 KO on blood pressure and inflammatory response were significantly reduced by S31-201 treatment. Circulating IL-9 levels were significantly increased in patients with the hypertension group than in the control group, and elevated IL-9 levels positively correlated with both systolic blood pressure and diastolic blood pressure in patients with hypertension. Conclusions. IL-9 KO alleviates inflammatory response, prevents phenotypic transformation of smooth muscle, reduces vascular dysfunction, and lowers blood pressure via the STAT3 pathway in Ang II-infused mice. IL-9 might be a novel target for the treatment and prevention of clinical hypertension.

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Section: Cd4+ T Helper (Th) Cells Include Regulatory T Cells (Treg) Amentioning

confidence: 73%

Interleukin-9 Deletion Relieves Vascular Dysfunction and Decreases Blood Pressure via the STAT3 Pathway in Angiotensin II-Treated Mice

Yang

Tang

Zhai

et al. 2020

Mediators of Inflammation

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“…FACS analysis indicated a marked increase in Th17 cells in HTN that was reversed by butyrate (Figure 8D). Th17 cells have critical roles in chronic inflammation in both animals and human [51–53]. Interestingly, most of the increased Th17 cells in mice intestine were CCR2 + cells known to be more proinflammatory, producing high levels of GM-CSF/IFN-γ and IL-17 [54,55].…”

Section: Resultsmentioning

confidence: 99%

Imbalance of gut microbiome and intestinal epithelial barrier dysfunction in patients with high blood pressure

et al. 2018

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Recent evidence indicates a link between gut pathology and microbiome with hypertension (HTN) in animal models. However, whether this association exists in humans is unknown. Thus, our objectives in the present study were to test the hypotheses that high blood pressure (BP) patients have distinct gut microbiomes and that gut–epithelial barrier function markers and microbiome composition could predict systolic BP (SBP). Fecal samples, analyzed by shotgun metagenomics, displayed taxonomic and functional changes, including altered butyrate production between patients with high BP and reference subjects. Significant increases in plasma of intestinal fatty acid binding protein (I-FABP), lipopolysaccharide (LPS), and augmented gut-targetting proinflammatory T helper 17 (Th17) cells in high BP patients demonstrated increased intestinal inflammation and permeability. Zonulin, a gut epithelial tight junction protein regulator, was markedly elevated, further supporting gut barrier dysfunction in high BP. Zonulin strongly correlated with SBP (R2 = 0.5301, P<0.0001). Two models predicting SBP were built using stepwise linear regression analysis of microbiome data and circulating markers of gut health, and validated in a separate cohort by prediction of SBP from zonulin in plasma (R2 = 0.4608, P<0.0001). The mouse model of HTN, chronic angiotensin II (Ang II) infusion, was used to confirm the effects of butyrate and gut barrier function on the cardiovascular system and BP. These results support our conclusion that intestinal barrier dysfunction and microbiome function are linked to HTN in humans. They suggest that manipulation of gut microbiome and its barrier functions could be the new therapeutic and diagnostic avenues for HTN.

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“…Older age, obesity and hypertension have previously been identified as EP risk factors, but the precise underlying mechanism of how these factors may cause EP is unclear . Interestingly, CD4 + T cell imbalance toward the proinflammatory Th17 subtype was previously observed to increase with age and was present in patients with obesity and hypertension . Therefore, a common immunity‐associated pathway might contribute to EP development as well as EP risk factors.…”

Section: Discussionmentioning

confidence: 99%

“…2,7,12 Interestingly, CD4 + T cell imbalance toward the proinflammatory Th17 subtype was previously observed to increase with age and was present in patients with obesity and hypertension. [19][20][21] Therefore, a common immunity-associated pathway might contribute to EP development as well as EP risk factors.…”

Section: Risk Of Ep Recurrence Was Associated With Cd4 + T Cell Imbmentioning

confidence: 99%

CD4⁺ T cell imbalance is associated with recurrent endometrial polyps

Zhu

et al. 2018

Clin Exp Pharma Physio

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Endometrial polyps (EPs) are localized benign overgrowths at the endometrium, with currently unknown aetiology and pathogenesis. Although symptoms of EP can be alleviated or resolved by hysteroscopic polypectomy, a significant fraction of individuals develop recurrent EPs after initial EP removal. In rare cases, EPs may also undergo malignant transformation. In-depth understanding of the mechanisms that are involved in EP development is urgently needed. Recent works indicate that dysregulations in the immune system participate in the development of a variety of symptoms, such as aging, obesity and hypertension, many of which are EP risk factors. Based on these discoveries, we investigated the cellular immune system in premenopausal women with and without EP. Compared to EP-free controls, the women with EP presented significantly higher RORC expression but unchanged TBX21 and FOXP3 expression in the circulating CD4 T cells. When stimulated with PMA/ionomycin, CD4 T cells from women with EP presented significantly higher interferon (IFN)-γ and interleukin (IL)-17 secretion, and lower transforming growth factor (TGF)-β secretion. Hysteroscopic polypectomy did not significantly alter the composition of CD4 T cells, as the women with EP presented a similar upregulation of Th17 inflammation and a downregulation of regulatory T cell (Treg) response postoperatively. Notably, in women that developed recurrent EP, the CD4 T cells presented higher preoperative and postoperative RORC, IFN-γ, and IL-17 expression, as well as lower postoperative FOXP3 and TGF-β expression, than hysteroscopic polypectomy-treated women without EP recurrence. These data demonstrated an association between CD4 T cell imbalance and recurrent EP development.

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Circulating Th1, Th2, and Th17 Levels in Hypertensive Patients

Cited by 60 publications

References 29 publications

Interleukin-9 Deletion Relieves Vascular Dysfunction and Decreases Blood Pressure via the STAT3 Pathway in Angiotensin II-Treated Mice

Interleukin-9 Deletion Relieves Vascular Dysfunction and Decreases Blood Pressure via the STAT3 Pathway in Angiotensin II-Treated Mice

Imbalance of gut microbiome and intestinal epithelial barrier dysfunction in patients with high blood pressure

CD4⁺ T cell imbalance is associated with recurrent endometrial polyps

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Circulating Th1, Th2, and Th17 Levels in Hypertensive Patients

Cited by 60 publications

References 29 publications

Interleukin-9 Deletion Relieves Vascular Dysfunction and Decreases Blood Pressure via the STAT3 Pathway in Angiotensin II-Treated Mice

Interleukin-9 Deletion Relieves Vascular Dysfunction and Decreases Blood Pressure via the STAT3 Pathway in Angiotensin II-Treated Mice

Imbalance of gut microbiome and intestinal epithelial barrier dysfunction in patients with high blood pressure

CD4+ T cell imbalance is associated with recurrent endometrial polyps

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CD4⁺ T cell imbalance is associated with recurrent endometrial polyps