Immunosenescence and inflammation characterize chronic heart failure patients with more advanced disease

Moro-García, Marco Antonio; Echeverría, Ainara; Galán-Artímez, María Concepción; Suárez-García, Francisco Manuel; Solano-Jaurrieta, Juan José; Avanzas, Pablo; Díaz‐Molina, Beatriz; Lambert, José Luis; López‐Larrea, Carlos; Morís, César; Alonso-Arias, Rebeca

doi:10.1016/j.ijcard.2014.04.128

Cited by 53 publications

(39 citation statements)

References 36 publications

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“…Patients with more advanced heart failure, as reflected by low AT, demonstrate an increased number of neutrophils. This relative neutrophilia is accompanied by a decreased number of lymphocytes, characterised by higher proportions of terminally differentiated CD4 + and CD8 + T-subsets [43]. These data are consistent with molecular mechanisms driving a T-cell immunosenescent state [44].…”

Section: Discussionsupporting

confidence: 57%

Cardiopulmonary Exercise Capacity and Preoperative Markers of Inflammation

Sultan

Edwards

Arroyo

et al. 2014

Mediators of Inflammation

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Explanatory mechanisms for the association between poor exercise capacity and infections following surgery are underexplored. We hypothesized that aerobic fitness—assessed by cardiopulmonary exercise testing (CPET)—would be associated with circulating inflammatory markers, as quantified by the neutrophil-lymphocyte ratio (NLR) and monocyte subsets. The association between cardiopulmonary reserve and inflammation was tested by multivariable regression analysis with covariates including anaerobic threshold (AT) and malignancy. In a first cohort of 240 colorectal patients, AT was identified as the sole factor associated with higher NLR (P = 0.03) and absolute and relative lymphopenia (P = 0.01). Preoperative leukocyte subsets and monocyte CD14+ expression (downregulated by endotoxin and indicative of chronic inflammation) were also assessed in two further cohorts of age-matched elective gastrointestinal and orthopaedic surgical patients. Monocyte CD14+ expression was lower in gastrointestinal patients (n = 43) compared to age-matched orthopaedic patients (n = 31). The circulating CD14+CD16− monocyte subset was reduced in patients with low cardiopulmonary reserve. Poor exercise capacity in patients without a diagnosis of heart failure is independently associated with markers of inflammation. These observations suggest that preoperative inflammation associated with impaired cardiorespiratory performance may contribute to the pathophysiology of postoperative outcome.

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Section: Discussionsupporting

confidence: 57%

Cardiopulmonary Exercise Capacity and Preoperative Markers of Inflammation

Sultan

Edwards

Arroyo

et al. 2014

Mediators of Inflammation

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“…It has been long recognized that myocardial aging is associated with increased interstitial fibrosis, hypertrophy, inflammation, stiffness, and mild contractile dysfunction (25). Several mechanisms have been proposed to explain this condition, including mitochondrial impairment (43), cardiomyocyte intrinsic factors (25), and deregulated immune responses (44)(45)(46).…”

Section: Discussionmentioning

confidence: 99%

Myocardial aging as a T-cell–mediated phenomenon

Ramos

Berg²,

Silva

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

142

117

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In recent years, the myocardium has been rediscovered under the lenses of immunology, and lymphocytes have been implicated in the pathogenesis of cardiomyopathies with different etiologies. Aging is an important risk factor for heart diseases, and it also has impact on the immune system. Thus, we sought to determine whether immunological activity would influence myocardial structure and function in elderly mice. Morphological, functional, and molecular analyses revealed that the age-related myocardial impairment occurs in parallel with shifts in the composition of tissueresident leukocytes and with an accumulation of activated CD4 + Foxp3 − (forkhead box P3) IFN-γ + T cells in the heart-draining lymph nodes. A comprehensive characterization of different aged immune-deficient mouse strains revealed that T cells significantly contribute to age-related myocardial inflammation and functional decline. Upon adoptive cell transfer, the T cells isolated from the mediastinal lymph node (med-LN) of aged animals exhibited increased cardiotropism, compared with cells purified from young donors or from other irrelevant sites. Nevertheless, these cells caused rather mild effects on cardiac functionality, indicating that myocardial aging might stem from a combination of intrinsic and extrinsic (immunological) factors. Taken together, the data herein presented indicate that heart-directed immune responses may spontaneously arise in the elderly, even in the absence of a clear tissue damage or concomitant infection. These observations might shed new light on the emerging role of T cells in myocardial diseases, which primarily affect the elderly population.T he myocardial cellular composition has been revisited in recent years, and leukocyte subsets residing in the healthy heart have been described (1-10). Cardiac-resident macrophages exhibiting an M2-like gene expression profile were found to be distributed in close association with the coronary vascular bed (3), and niches for dendritic cells (CD11c + MHC-II high CD80/86 low ) were found near the cardiac valves of the intact heart (1). It was also demonstrated that cardiac-resident MHCII + cells process and present myosin heavy chain-alpha-derived peptides under steady-state conditions (11, 12) and prime T cells ex vivo (1). However, whether lymphocytes can seed the intact myocardium and whether T-cell priming with myocardial antigens can occur in the absence of an infection or autoimmune myocarditis remain elusive.More recently, accumulating evidence indicated that noninfectious myocardial diseases are modulated by T cells. During the last couple of years, our group demonstrated that ischemic, sterile myocardial injuries can elicit lymphocyte activation directed against cardiac antigens (13-16). Our previous data, showing for the first time that CD4 + T cells reactive to cardiac components can foster the healing process that takes place after myocardial infarction, were corroborated by several other reports (13,15,(17)(18)(19)(20). However, these autoreactive T cells can also b...

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“…Chronic heart failure (CHF), a form of cardiovascular disease prevalent in the elderly, has also been associated with a state of chronic inflammation . High levels of pro‐inflammatory cytokines: TNF, IL‐1 β and IL‐6 have been detected in patient myocardium and peripheral tissues . Furthermore, it was shown that pro‐inflammatory cytokine levels in the plasma affect clinical outcomes, as patients with higher levels of IL‐6 were associated with worse CHF pathogenesis .…”

Section: Effects Of Immunosenescence In Other Age‐related Diseasesmentioning

confidence: 99%

“…155 Furthermore, it was shown that pro-inflammatory cytokine levels in the plasma affect clinical outcomes, as patients with higher levels of IL-6 were associated with worse CHF pathogenesis. 155 In addition, the expression of Toll-like receptor-4 (TLR4) receptor, as well as TLR4associated pro-inflammatory cytokines, were shown to be increased in hearts of patients with CHF. 156 The contribution of TLR4 expression towards CHF pathogenesis was also reported in another finding, with increased levels of TLR4 expression on monocytes in patients with CHF.…”

Section: Effects Of Immunosenescence In Other Age-related Diseasesmentioning

confidence: 99%

Age has a role in driving host immunopathological response to alphavirus infection

Chan

2017

Immunology

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SummaryAlphaviruses are a group of arthropod-borne pathogens capable of causing a wide spectrum of clinical symptoms, ranging from milder symptoms like rashes, fever and polyarthralgia, to life-threatening encephalitis. This genus of viruses is prevalent globally, and can infect patients across a wide age range. Interestingly, disease severity of virus-infected patients is wideranging. Definitions of the pathogenesis of alphaviruses, as well as the host factors influencing disease severity, remain limited. The innate and adaptive immune systems are important host defences against alphavirus infections. Several reports have highlighted the roles of specific immune subsets in contributing to the immune pathogenesis of these viruses. However, immunosenescence, a gradual deterioration of the immune system brought about by the natural advancement of age, affects the functional roles of these immune subsets. This phenomenon compromises the host's ability to defend against alphavirus infection and pathogenesis. In addition, the lack of maturity in the immune system in newborns and infants also results in more severe disease outcomes. In this review, we will summarize the subtle yet diverse physiological changes in the immune system during aging, and how these changes underlie the differences in disease severity for common alphaviruses.

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Immunosenescence and inflammation characterize chronic heart failure patients with more advanced disease

Cited by 53 publications

References 36 publications

Cardiopulmonary Exercise Capacity and Preoperative Markers of Inflammation

Cardiopulmonary Exercise Capacity and Preoperative Markers of Inflammation

Myocardial aging as a T-cell–mediated phenomenon

Age has a role in driving host immunopathological response to alphavirus infection

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