scholarly journals Depletion of β3-adrenergic receptor relieves pressure overload-induced cardiac hypertrophy and heart failure via enhancing innate immune response

2021 ◽  
Vol 143 ◽  
pp. 112194
Author(s):  
Xuemei Wei ◽  
Andi Zhang ◽  
Wenbo Yang ◽  
Yuehua Fang
PLoS ONE ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. e0243788
Author(s):  
Christina Katharina Weisheit ◽  
Jan Lukas Kleiner ◽  
Maria Belen Rodrigo ◽  
Sven Thomas Niepmann ◽  
Sebastian Zimmer ◽  
...  

The CX3CL1/CX3CR1 axis mediates recruitment and extravasation of CX3CR1-expressing subsets of leukocytes and plays a pivotal role in the inflammation-driven pathology of cardiovascular disease. The cardiac immune response differs depending on the underlying causes. This suggests that for the development of successful immunomodulatory therapy in heart failure due to chronic pressure overload induced left ventricular (LV) hypertrophy, the underlying immune patterns must be examined. Here, the authors demonstrate that Fraktalkine-receptor CX3CR1 is a prerequisite for the development of cardiac hypertrophy and left ventricular dysfunction in a mouse model of transverse aortic constriction (TAC). The comparison of C57BL/6 mice with CX3CR1 deficient mice displayed reduced LV hypertrophy and preserved cardiac function in response to pressure overload in mice lacking CX3CR1. Moreover, the normal immune response following TAC induced pressure overload which is dominated by Ly6Clow macrophages changed to an early pro-inflammatory immune response driven by neutrophils, Ly6Chigh macrophages and altered cytokine expression pattern in CX3CR1 deficient mice. In this early inflammatory phase of LV hypertrophy Ly6Chigh monocytes infiltrated the heart in response to a C-C chemokine ligand 2 burst. CX3CR1 expression impacts the immune response in the development of LV hypertrophy and its absence has clear cardioprotective effects. Hence, suppression of CX3CR1 may be an important immunomodulatory therapeutic target to ameliorate pressure-overload induced heart failure.


2011 ◽  
Vol 2 (1) ◽  
pp. 2 ◽  
Author(s):  
Jennifer A Onyimba ◽  
Michael J Coronado ◽  
Amanda E Garton ◽  
Joseph B Kim ◽  
Adriana Bucek ◽  
...  

2015 ◽  
Vol 29 (3) ◽  
pp. 119-129 ◽  
Author(s):  
Richard J. Stevenson ◽  
Deborah Hodgson ◽  
Megan J. Oaten ◽  
Luba Sominsky ◽  
Mehmet Mahmut ◽  
...  

Abstract. Both disgust and disease-related images appear able to induce an innate immune response but it is unclear whether these effects are independent or rely upon a common shared factor (e.g., disgust or disease-related cognitions). In this study we directly compared these two inductions using specifically generated sets of images. One set was disease-related but evoked little disgust, while the other set was disgust evoking but with less disease-relatedness. These two image sets were then compared to a third set, a negative control condition. Using a wholly within-subject design, participants viewed one image set per week, and provided saliva samples, before and after each viewing occasion, which were later analyzed for innate immune markers. We found that both the disease related and disgust images, relative to the negative control images, were not able to generate an innate immune response. However, secondary analyses revealed innate immune responses in participants with greater propensity to feel disgust following exposure to disease-related and disgusting images. These findings suggest that disgust images relatively free of disease-related themes, and disease-related images relatively free of disgust may be suboptimal cues for generating an innate immune response. Not only may this explain why disgust propensity mediates these effects, it may also imply a common pathway.


Pneumologie ◽  
2013 ◽  
Vol 67 (S 01) ◽  
Author(s):  
P Pfeifer ◽  
M Voss ◽  
B Wonnenberg ◽  
M Bischoff ◽  
F Langer ◽  
...  

2016 ◽  
Vol 54 (12) ◽  
pp. 1343-1404
Author(s):  
C Cai ◽  
B Koch ◽  
S Akhras ◽  
E Hildt ◽  
S Zeuzem ◽  
...  

2008 ◽  
Vol 46 (01) ◽  
Author(s):  
Y Malato ◽  
N Beraza ◽  
LE Sander ◽  
L Sander ◽  
M Al-Masaoudi ◽  
...  

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