Allergic asthma accelerates atherosclerosis dependent on Th2 and Th17 in apolipoprotein E deficient mice

Wang, Lijun; Gao, Shanshan; Xu, Wei; Zhao, Sijia; Zhou, Juan; Wang, Nanping; Yuan, Zuyi

doi:10.1016/j.yjmcc.2014.02.005

Cited by 37 publications

(30 citation statements)

References 36 publications

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“…In apolipoprotein E-deficient ( Apoe − / − ) mice, development of allergic airway inflammation significantly enlarged atherosclerotic plaques and increased lesion inflammation. 29 Recent data from the Multi-Ethnic Study of Atherosclerosis show that asthmatic patients who use inhaled corticosteroids, leukotriene inhibitors, or oral corticosteroids have significantly higher plasma C-reactive protein and fibrinogen concentrations, lower unadjusted cardiovascular disease (CVD)-free survival rate and higher CVD risk than asthmatic patients who do not use these medications or those without asthma. 26 Although atherosclerosis may not underlie all AAA, atherosclerosis usually accompanies aneurysmal dilation, 30 and constitutes a long-recognized risk factor of AAA.…”

Section: Discussionmentioning

confidence: 99%

Asthma Associates With Human Abdominal Aortic Aneurysm and Rupture

Liu

Wemmelund

Wang

et al. 2016

ATVB

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Objective Asthma and abdominal aortic aneurysms (AAA) both involve inflammation. It remains unknown whether these diseases interact. Approach and Results Databases analyzed included DNRP: a population-based nationwide case-control study included all patients with ruptured AAA (rAAA) and age- and sex-matched AAA controls without rupture in Denmark from 1996–2012. VIVA: Subgroup study of participants from the population-based randomized Viborg vascular screening trial. Asthmatic patients were categorized by hospital diagnosis, bronchodilator use, and the recorded use of other anti-asthma prescription medications. Logistic regression models were fitted to determine whether asthma associated with the risk of rAAA in DNRP, and an independent risk of having an AAA at screening in the VIVA trial. From the DNRP study, asthma diagnosed less than one year or six months before the index date increased the risk of AAA rupture before (odds ratio OR=1.60, 2.12) and after (OR=1.51, 2.06) adjusting for AAA comorbidities. Use of bronchodilators elevated the risk of AAA rupture from ever use to within 90 days from the index date, before (OR=1.10~1.37) and after (OR=1.10~1.31) adjustment. Patients prescribed anti-asthma drugs also showed an increased risk of rupture before (OR=1.12~1.79) and after (OR=1.09~1.48) the same adjustment. In VIVA, anti-asthmatic medication use associated with increased risk of AAA before (OR=1.45) or after adjustment for smoking (OR=1.45) or other risk factors (OR=1.46). Conclusions Recent active asthma increased risk of AAA and AAA-rupture. These findings document and furnish novel links between airway disease and AAA, two common diseases that share inflammatory aspects.

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Section: Discussionmentioning

confidence: 99%

Asthma Associates With Human Abdominal Aortic Aneurysm and Rupture

Liu

Wemmelund

Wang

et al. 2016

ATVB

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“…The role of IL-4 in atherosclerosis remains more controversial. Some studies have indirectly implicated IL-4 as pro-atherosclerotic [15,16], although others found little or no effect on disease in Apoe −/− ; Il-4 −/− mice reconstituted with Il-4 −/− bone marrow [17]. …”

Section: Atherosclerosismentioning

confidence: 99%

I-L-C-2 it: type 2 immunity and group 2 innate lymphoid cells in homeostasis

Moltke

Locksley

2014

Current Opinion in Immunology

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Innate type 2 immune cells are activated in response to helminths, allergens, and certain types of proteases and particulates. Recently, innate type 2 immune pathways have also been implicated in protective host responses to homeostatic perturbations, such as metabolic dysfunction, atherosclerosis, and tissue injury. In this context, innate type 2 cytokines stimulate local tissues, recruit eosinophils, and alternatively activate macrophages to restore homeostasis. As the major source of innate interleukin (IL)-5 and IL-13, group 2 innate lymphoid cells are positioned to initiate and maintain homeostatic type 2 responses. The absence of exogenous stimuli in these processes implicates endogenous pathways in the activation of type 2 immunity and suggests an alternative evolutionary trajectory for type 2 immunity, apart from its role in response to helminths and allergens.

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“…151 Ovalbumin-induced airway allergic inflammation increased atherosclerotic lesions in atherosclerosis-prone Apoe -/-mice, indicating a direct role for asthma in experimental atherosclerosis. 152 Cardiovascular diseases also increase the risk of severe and fatal anaphylactic episodes. 153 In a retrospective analysis, cardiovascular diseases were found in most patients with fatal anaphylaxis 154 and, in an autopsy study of patients with fatal anaphylaxis, most had coronary artery disease or cardiomyopathy.…”

Section: The Complement Systemmentioning

confidence: 99%

Mast cells in human and experimental cardiometabolic diseases

2015

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Mast cells, like many other types of inflammatory cell, perform pleiotropic roles in cardiometabolic diseases such as atherosclerosis, abdominal aortic aneurysms, obesity, and diabetes mellitus, as well as complications associated with these diseases. Low numbers of mast cells are present in the heart, aorta, and adipose tissue of healthy humans, but patients with cardiometabolic diseases and animals with experimentally-induced cardiometabolic pathologies have high numbers of mast cells with increased activity in the affected tissues. Mediators released by the activated mast cells, such as chemokines, cytokines, growth factors, heparin, histamine, and proteases, not only function as biomarkers of cardiometabolic diseases, but might also directly contribute to the pathogenesis of such diseases. Mast-cell mediators impede the functions of vascular cells, the integrity of the extracellular matrix, and the activity of other inflammatory cells, thereby contributing to the pathobiology of the conditions at multiple levels. In mouse models, mast-cell activation aggravates the progression of various cardiometabolic pathologies, whereas a genetic deficiency or pharmacological stabilization of mast cells, or depletion or inhibition of specific mast-cell mediators, tends to delay the progression of such conditions. Pharmacological inhibition of mast-cell activation or their targeted effector functions offers potential novel therapeutic strategies for patients with cardiometabolic disorders.

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Allergic asthma accelerates atherosclerosis dependent on Th2 and Th17 in apolipoprotein E deficient mice

Cited by 37 publications

References 36 publications

Asthma Associates With Human Abdominal Aortic Aneurysm and Rupture

Asthma Associates With Human Abdominal Aortic Aneurysm and Rupture

I-L-C-2 it: type 2 immunity and group 2 innate lymphoid cells in homeostasis

Mast cells in human and experimental cardiometabolic diseases

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