Context: Current investigations illustrate the increasing prevalence of atherosclerosis (AS) through the aggravating role of inappropriate lifestyle patterns. Atherosclerosis is the cause of important vascular-related diseases such as ischemic stroke (IS). Understanding AS pathophysiology can help reduce the incidence of AS-mediated diseases like ischemic stroke. Evidence Acquisition: For this narrative review article, we used the five mega databases of PubMed, Google Scholar, Scopus, Springer, and Science Direct. We searched from 2010 Jan to 2020 Dec and based on keywords and inclusion criteria, 77 articles were enrolled. Results: Based on prior articles on atherosclerosis and ischemic stroke pathophysiology, local and systemic inflammation is a vigorous factor in both diseasesIndeed, the fundamental inflammatory pathway involved atherosclerosis, and ischemic stroke is associated with the toll-like receptor 4/myeloid differentiation primary response 88/nuclear factor-kappa B (TLR4/ Myd88/ NF-κB) cascade. The functional paw of these intricate mechanisms are pro-inflammatory mediators, such as interleukin-1 beta (IL-1β), tumor necrosis factor (TNF-α), and interleukin-18 (IL-18) incite inflammation. Besides, the essential structures termed inflammasomes (multi proteins components), and multiplicity of immune and non-immune cells (i.e., neutrophils, monocytes, platelets, and macrophages) are beneficial in the induction of inflammatory microenvironment. Conclusions: Neutrophils could be the most effective cells in the inflammation-based mechanism in IS and AS. It is clarified that neutrophils with the recruitment of own vesicles and granules can afford to amplify inflammatory conditions and be a key cell in AS and IS cross-talk. Therefore, utilizing methods to control neutrophils-mediated mechanisms could be an effective method for the prevention of AS and IS.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a member of the Coronaviridae family that causes the novel coronavirus disease (COVID-19). SARS-CoV-2 is an RNA enveloped virus that firstly emerged in Wuhan, China, in December 2019 over the 21st century. It is rapidly spread by human-to-human transmission through droplets or airborne particles. COVID-19 can be complicated by acute respiratory distress syndrome (ARDS) and severe pneumonia, depending on ACE2 and Spike protein (as viral surface protein). It is required a proper defense mechanism for the body to be healthy in fighting back against infectious diseases, especially COVID-19. Since there are no wholly approved drugs, vaccines, or clinical prevention for this disease at the moment, it is essential to focus on natural resistance systems, which play critical roles in supporting the immune system defense function against COVID-19. The severity of COVID-19 is characterized by an increase in acute phase reactants and pro-inflammatory cytokines; ferritin, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and IL-1β. Numerous shreds of evidence propose that immune homeostasis, genetic susceptibility, dietary interventions, supplementation, and the environment can have an imperative role in controlling the severity of SARS-CoV-2 infection and infected patients’ prognosis. In the current study, we proposed a comprehensive overview of the considerable part of natural resistance in the COVID-19 forecast, whether it may afford protection to COVID-19. All in all, multidisciplinary investigations have been done and need to be done to identify the clinical implications of natural interventions and natural resistance potential in COVID-19 susceptibility

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