The possible pathophysiology mechanism of cytokine storm in elderly adults with COVID-19 infection: the contribution of "inflame-aging"

被引:205
作者
Meftahi, Gholam Hossein [1 ]
Jangravi, Zohreh [2 ]
Sahraei, Hedayat [1 ]
Bahari, Zahra [1 ,3 ]
机构
[1] Baqiyatallah Univ Med Sci, Neurosci Res Ctr, Tehran, Iran
[2] Baqiyatallah Univ Med Sci, Dept Biochem, Fac Med, Tehran, Iran
[3] Baqiyatallah Univ Med Sci, Dept Physiol & Med Phys, Fac Med, Tehran 1435916471, Iran
关键词
ACE2; receptor; Autophagy; COVID-19; Cytokine storm; Senescent cell; Vitamin D; IMMUNE CELLS; VITAMIN-D; STRESS; INFLAMMATION; AUTOPHAGY; CANCER;
D O I
10.1007/s00011-020-01372-8
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Purpose Novel Coronavirus disease 2019 (COVID-19), is an acute respiratory distress syndrome (ARDS), which is emerged in Wuhan, and recently become worldwide pandemic. Strangely, ample evidences have been shown that the severity of COVID-19 infections varies widely from children (asymptomatic), adults (mild infection), as well as elderly adults (deadly critical). It has proven that COVID-19 infection in some elderly critical adults leads to a cytokine storm, which is characterized by severe systemic elevation of several pro-inflammatory cytokines. Then, a cytokine storm can induce edematous, ARDS, pneumonia, as well as multiple organ failure in aged patients. It is far from clear till now why cytokine storm induces in only COVID-19 elderly patients, and not in young patients. However, it seems that aging is associated with mild elevated levels of local and systemic pro-inflammatory cytokines, which is characterized by "inflamm-aging". It is highly likely that "inflamm-aging" is correlated to increased risk of a cytokine storm in some critical elderly patients with COVID-19 infection. Methods A systematic search in the literature was performed in PubMed, Scopus, Embase, Cochrane Library, Web of Science, as well as Google Scholar pre-print database using all available MeSH terms for COVID-19, Coronavirus, SARS-CoV-2, senescent cell, cytokine storm, inflame-aging, ACE2 receptor, autophagy, and Vitamin D. Electronic database searches combined and duplicates were removed. Results The aim of the present review was to summarize experimental data and clinical observations that linked the pathophysiology mechanisms of "inflamm-aging", mild-grade inflammation, and cytokine storm in some elderly adults with severe COVID-19 infection.
引用
收藏
页码:825 / 839
页数:15
相关论文
共 116 条
[1]  
Agrawal A, 2009, DNA J IMMUNOL, V182, p2 1138 1145
[2]   Immunosenescence and Its Hallmarks: How to Oppose Aging Strategically? A Review of Potential Options for Therapeutic Intervention [J].
Aiello, Anna ;
Farzaneh, Farzin ;
Candore, Giuseppina ;
Caruso, Calogero ;
Davinelli, Sergio ;
Gambino, Caterina Maria ;
Ligotti, Mattia Emanuela ;
Zareian, Nahid ;
Accardi, Giulia .
FRONTIERS IN IMMUNOLOGY, 2019, 10
[3]   Age-dependent impairment of adipose-derived stem cells isolated from horses [J].
Alicka, Michalina ;
Kornicka-Garbowska, Katarzyna ;
Kucharczyk, Katarzyna ;
Kepska, Martyna ;
Rocken, Michael ;
Marycz, Krzysztof .
STEM CELL RESEARCH & THERAPY, 2020, 11 (01)
[4]  
Alves AS, 2019, EINSTEIN-SAO PAULO, V17, P5
[5]  
Aslam MM, 2019, BIOMED RES INT-UK, V2019, P12
[6]   Dopamine effects on stress-induced working memory deficits [J].
Bahari, Zahra ;
Meftahi, Gholam H. ;
Meftahi, Mohammad A. .
BEHAVIOURAL PHARMACOLOGY, 2018, 29 (07) :584-591
[7]   Regulation of Dendritic Cell Function by Vitamin D [J].
Barragan, Myriam ;
Good, Misty ;
Kolls, Jay K. .
NUTRIENTS, 2015, 7 (09) :8127-8151
[8]   Human T cell immunosenescence and inflammation in aging [J].
Bektas, Arsun ;
Schurman, Shepherd H. ;
Sen, Ranjan ;
Ferrucci, Luigi .
JOURNAL OF LEUKOCYTE BIOLOGY, 2017, 102 (04) :977-988
[9]   Does the Interdependence between Oxidative Stress and Inflammation Explain the Antioxidant Paradox? [J].
Biswas, Subrata Kumar .
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY, 2016, 2016
[10]   Mechanisms of Disease: Telomere Diseases. [J].
Calado, Rodrigo T. ;
Young, Neal S. .
NEW ENGLAND JOURNAL OF MEDICINE, 2009, 361 (24) :2353-2365