scholarly journals Polymorbidity, ageing of immune system and low-grade systemic inflammation: a challenge for modern medicine

2020 ◽  
Vol 22 (4) ◽  
pp. 609-624
Author(s):  
V. S. Shirinsky ◽  
I. V. Shirinsky

The  review  article  considers the  data  from  literature that  concern polymorbidity aspects,  its interrelations with ageing of immune system and lo-grade immune ageing, mechanisms of genesis, approaches to its prevention and treatment. Evolution of “comorbidity” and “polymorbidity” terms is traced, an updated definition of polymorbidity is proposed. The  world-wide incidence of polymorbidity is increased and  now it reaches  23-25%  in general  population, and up to 98%, in elderly people  (> 65 years old).  The risk factors  of polymorbidity are considered, like as its social burden due to high costs for healthcare, high mortality rates, excessive treatment provided by multidisciplinary specialists.  We present  evidence  for common molecular and cellular  mechanisms involved  in ageing and polymorbidity, being unified  by the term  “inflammaging” which represents a low-grade chronic systemic  inflammation associated with  ageing.  The  data  are  presented that concern the “inflammaging” development with involvement of ageing cells from innate and adaptive immunity systems,  different   pro and  anti-inflammatory mediators, lifelong  antigenic load.  The  data  are  analyzed concerning functional and  structural changes  in the  inborn and  adaptive  immune system  in ageing,  role of these changes  in “inflammaging” persistence and development of polymorbid conditions. There  are complex interactions shown between  the bodily senescence and immune ageing, with similar underlying mechanisms in some cases, however, being quite different  in other  instances. With age, upon  existing risk factors,  the changed adaptive  immunity in most people  is not able to full-scale  coping  with chronic antigenic load,  thus increasing the risk of diseases. Moreover, in many elderly people these changes are compensated by steady activation of the innate immunity cells. It is noted  that the aging events and development of disease (polymorbidity) cannot be considered distinct entities, since they can interact, being, however, basically different in their nature. In future, one should concentrate our efforts on elucidation of molecular and cellular mechanisms of these interactions, solution of the  tasks  oriented for development of such  interventions that  could  be able  to  reduce  harmful consequences of ageing and to use useful effects for health  maintenance and reaching maximal longevity.

Sports ◽  
2021 ◽  
Vol 9 (9) ◽  
pp. 121
Author(s):  
Johan Jakobsson ◽  
Ian Cotgreave ◽  
Maria Furberg ◽  
Niklas Arnberg ◽  
Michael Svensson

The coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has unmasked mankind’s vulnerability to biological threats. Although higher age is a major risk factor for disease severity in COVID-19, several predisposing risk factors for mortality are related to low cardiorespiratory and metabolic fitness, including obesity, cardiovascular disease, diabetes, and hypertension. Reaching physical activity (PA) guideline goals contribute to protect against numerous immune and inflammatory disorders, in addition to multi-morbidities and mortality. Elevated levels of cardiorespiratory fitness, being non-obese, and regular PA improves immunological function, mitigating sustained low-grade systemic inflammation and age-related deterioration of the immune system, or immunosenescence. Regular PA and being non-obese also improve the antibody response to vaccination. In this review, we highlight potential physiological, cellular, and molecular mechanisms that are affected by regular PA, increase the host antiviral defense, and may determine the course and outcome of COVID-19. Not only are the immune system and regular PA in relation to COVID-19 discussed, but also the cardiovascular, respiratory, renal, and hormonal systems, as well as skeletal muscle, epigenetics, and mitochondrial function.


2021 ◽  
Vol 22 (22) ◽  
pp. 12539
Author(s):  
Ludmila Müller ◽  
Svetlana Di Benedetto

Aging is characterized by the dynamic remodeling of the immune system designated “immunosenescence,” and is associated with altered hematopoiesis, thymic involution, and lifelong immune stimulation by multitudinous chronic stressors, including the cytomegalovirus (CMV). Such alterations may contribute to a lowered proportion of naïve T-cells and to reduced diversity of the T-cell repertoire. In the peripheral circulation, a shift occurs towards accumulations of T and B-cell populations with memory phenotypes, and to accumulation of putatively senescent and exhausted immune cells. The aging-related accumulations of functionally exhausted memory T lymphocytes, commonly secreting pro-inflammatory cytokines, together with mediators and factors of the innate immune system, are considered to contribute to the low-grade inflammation (inflammaging) often observed in elderly people. These senescent immune cells not only secrete inflammatory mediators, but are also able to negatively modulate their environments. In this review, we give a short summary of the ways that immunosenescence, inflammaging, and CMV infection may cause insufficient immune responses, contribute to the establishment of the hyperinflammatory syndrome and impact the severity of the coronavirus disease 2019 (COVID-19) in elderly people.


2021 ◽  
Vol 11 ◽  
Author(s):  
Shireen Mohammad ◽  
Christoph Thiemermann

Diet-induced metabolic endotoxemia is an important factor in the development of many chronic diseases in animals and man. The gut epithelium is an efficient barrier that prevents the absorption of liposaccharide (LPS). Structural changes to the intestinal epithelium in response to dietary alterations allow LPS to enter the bloodstream, resulting in an increase in the plasma levels of LPS (termed metabolic endotoxemia). LPS activates Toll-like receptor-4 (TLR4) leading to the production of numerous pro-inflammatory cytokines and, hence, low-grade systemic inflammation. Thus, metabolic endotoxemia can lead to several chronic inflammatory conditions. Obesity, diabetes, and non-alcoholic fatty liver disease (NAFLD) can also cause an increase in gut permeability and potential pharmacological and dietary interventions could be used to reduce the chronic low-grade inflammation associated with endotoxemia.


Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4472
Author(s):  
Constanza C. Astudillo-López ◽  
Natividad Castro-Alarcón ◽  
Ana C. Ariza ◽  
José F. Muñoz-Valle ◽  
Ulises de la Cruz-Mosso ◽  
...  

A western diet and increased intestinal permeability may contribute to systemic inflammation and the development of cardio-metabolic alterations. The aim of this study was to assess the relationship between diet, biomarkers of intestinal permeability, and chronic low-grade inflammation on the cardiometabolic profile. A cross-sectional study was carried out in 238 young subjects aged 18–29 years, divided into two groups: with <3 cardiometabolic risk factors (CRF) and ≥3 risk factors. Anthropometric parameters, biochemical profile, and serum levels of zonulin, lipopolysaccharide (LPS), and high-sensitivity C-reactive protein (hs-CRP) were measured, and the macronutrient intake was evaluated. Interaction models showed elevated glucose levels in the presence of high biomarker levels: zonulin ≥51.6 ng/mL plus LPS ≥ 1.35 EU/mL (β = 1.1, p = 0.006), and LPS ≥1.35 EU/mL plus hs-CRP ≥ 4.3 mg/L (β = 1.2, p = 0.007). In addition, triglyceride levels increased in the presence of LPS ≥ 1.35 EU/mL and hs-CRP ≥ 4.3 mg/L (β = 3.9, p = 0.01). Despite having increased biomarker levels, a higher consumption of water (≥2100 mL), polyunsaturated fatty acids (≥60 g), or fiber (≥30 g) decreased triglyceride (β = −9.6, p = 0.03), total cholesterol (β = −5.1, p = 0.01), and LDL-C levels (β = −7.7, p = 0.01). These findings suggest that the increased consumption of water, PUFA and fiber may improve lipid profile in subjects with intestinal permeability dysfunction or low-grade systemic inflammation.


GeroScience ◽  
2018 ◽  
Vol 40 (1) ◽  
pp. 61-69 ◽  
Author(s):  
Carlo Cervellati ◽  
Alessandro Trentini ◽  
Cristina Bosi ◽  
Giuseppe Valacchi ◽  
Mario Luca Morieri ◽  
...  

2004 ◽  
Vol 24 (4) ◽  
pp. 327-339 ◽  
Author(s):  
Roberto Pecoits–Filho ◽  
Peter Stenvinkel ◽  
Angela Yee-Moon Wang ◽  
Olof Heimbürger ◽  
Bengt Lindholm

Mortality and morbidity in chronic kidney disease (CKD) patients are unacceptably high. The annual mortality rate due to cardiovascular disease (CVD) is approximately 9%, which, for the middle-aged person, is at least 10- to 20-fold higher than for the general population. Classic risk factors for CVD are highly prevalent in CKD patients, but they cannot fully account for the excessive rate of CVD in this population. Instead, it has become increasingly clear that nontraditional risk factors, such as systemic inflammation, may play a key role in the development of atherosclerosis. It is well established that inflammatory markers are very powerful predictors of high CVD morbidity and mortality not only in the general population, but particularly in CKD patients. Signs of a sustained low-grade inflammation, such as increased levels of C-reactive protein (CRP), are present in the majority of stage 5 CKD patients, even in patients in clinically stable condition, and they are also commonly observed after the initiation of dialysis therapy. Dialysis therapy — hemodialysis as well as peritoneal dialysis (PD) — may itself contribute to systemic inflammation. Local intraperitoneal inflammation can also occur in patients treated with PD. These local effects may result in a low-grade inflammation, caused by the bioincompatibility of conventional glucose-based dialysis fluids, to intense inflammation associated with peritonitis. Given these circumstances, it is reasonable to hypothesize that strategies aiming to reduce inflammation are potentially important and novel, and could serve to reduce CVD, thereby lowering morbidity and mortality in patients with CKD. In this review we provide information supporting the hypothesis that systemic inflammation is tightly linked to the most common complications of CKD patients, in particular those on PD, and that local inflammation in PD may contribute to various related complications. The aims of this review are to discuss the reasons that make inflammation an attractive target for intervention in CKD, the particular aspects of the inflammation–CVD axis during PD treatment that are likely involved, and possible means for the detection and management of chronic inflammation in PD patients.


Author(s):  
Thibault Teissier ◽  
Eric Boulanger ◽  
Lynne S Cox

Acute inflammation is a physiological response to injury or infection, with a cascade of steps that ultimately leads to recruitment of immune cells to clear invading pathogens and heal wounds. However, chronic inflammation arising from continued presence of the initial trigger, or dysfunction of signalling and/or effector pathways, is harmful to health. While successful ageing in older adults including centenarians is associated with low levels of inflammation, elevated inflammation increases the risk of poor health and death [1&ndash;3]. Hence inflammation has been described as one of seven pillars of ageing. Age-associated sterile, chronic, and low-grade inflammation is commonly termed inflammageing - it is not simply a consequence of increasing chronological age, but is also a marker of biological ageing, multimorbidity and mortality risk. While inflammageing was initially thought to be caused by &ldquo;continuous antigenic load and stress&rdquo;, reports from the last two decades describe a much more complex phenomenon also involving cellular senescence and ageing of the immune system. In this review, we explore the sources and consequences of inflammageing and highlight potential interventions. In particular, we assess the contribution of cellular senescence to age-associated inflammation, identify patterns of pro- and anti-inflammatory markers characteristic of inflammageing, describe alterations in the ageing immune system that lead to elevated inflammation, and finally assess the ways that diet, exercise and pharmacological interventions can reduce inflammageing and thus improve later life health.


2020 ◽  

Background: The outbreak of Coronavirus Disease 2019 (COVID-19) has led to a major concern for those who are more vulnerable to infections. Objectives: This study aimed to evaluate the most important risk factors for severe COVID-19 pneumonia. Methods: This retrospective study included information on clinical and epidemiological features of 105 patients with severe COVID-19 pneumonia hospitalized in Tajrish Hospital, Tehran, Iran. Initially, the medical records of the patients were investigated, and an interview was conducted based on a pre-prepared checklist to seek information about symptoms, past medical history, medication history, and behavior before hospitalization. Results: Out of 105 participants, 76 (72.5%) cases were male, and 54 (51.4%) patients were older than 54 years old. The majority of the patients (n=18; 17.1%) had both hypertension and diabetes (n=12; 11.4%). Metformin (n=36; 34.3%) was the most used medication amongst the studied patient. In addition, 24 (22.9%) patients were recreational hookah smokers, and the majority (75%) of them were under the age of 46 years old. Eventually, 19 patients were excluded from the study, of whom 11 individuals had diabetes, and 10 cases were using metformin. Conclusion: Apparently, hookah smoking played a critical role in the spread of COVID-19 in Iran and has made younger people more susceptible. In addition to older age, the immunosuppressive effects of Metformin seem to make diabetic patients with an impaired immune system more vulnerable to severe COVID-19 pneumonia. More studies on the immune system of vulnerable individuals by identifying their differences can help to protect them.


2014 ◽  
pp. 48-56
Author(s):  
Van Thi Tran ◽  
Van Bang Le ◽  
Thị Thu Huong Hoang

Aim: Some studies have linked the present of chronic obstructive oulmonary disease (COPD) to coronary artery disease (CAD). Low grade systemic inflammation occurs in patients with COPD as well as patients with CAD. This study was designed to find out the concentration differences of hs-CRP and TNF-a in patients having both chronic obstructive pulmonary and coronary artery diseases with those having either. Methods: A cross - sectional descriptive study was conducted in 200 patients undergoing a coronary artery angiography in the Heart Institute, Thong Nhat Hospital and 115 People Hospital. COPD was diagnosed using GOLD classification. Result: Our study had shown that the levels of hs-CRP and TNF-a were statistically increased in patients with COPD, CAD as well as in patients who had COPD with CAD (p<0,05). The levels of hs-CRP were higher in CAD than in COPD nad the levels of TNF-a were higher in COPD than in CAD. In patients with COPD and CAD, there were increased the levels of both hs-CRP and TNF-a in serum. Conclusion: Systemic inflammation presents in both COPD and CAD. Key words: hs-CRP, TNF-a, coronary artery disease (CAD).


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