Release of pro-inflammatory cytokines and activation of the innate immune system may be the result of either external (biological or chemical agents) or internal (genetic mutations/variations) factors. The cytokine Interleukin 6 and C-reactive protein are common inflammatory markers used to diagnose systemic inflammation risk.[3] Baseline C-reactive protein levels deviate due to natural genetic variation, but significant increases can result from risk factors such as smoking, obesity, lifestyle, and high blood pressure.[3] Excess advanced glycation end-products attach to RAGE receptors to produce chronic inflammation.[4]
It is firmly established that systemic markers for inflammation predict coronary heart disease complications with or without existing heart disease.[2] Inflammation also plays a role in diabetes risk and new research continues to support this conclusion.[7]Cancer is often caused by chronic inflammation.[8]
Research suggests chronic inflammation plays a major role in COVID-19 morbidity.[9][10] In severe cases, COVID-19 causes a cytokine storm which contributes to excessive and uncontrolled inflammation of organs, particularly respiratory tissues.[11][12] If untreated, this increased inflammation can result in reduced immune response, pneumonia, lymphoid tissue damage, and death.[11] Individuals with abnormal cytokine production, such as those with obesity or systemic chronic inflammation, have poorer health outcomes from COVID-19.[9][10] Elevated cytokine production alters the innate immune response which leads to abnormal T-cell and B-Cell function that decreases control of viral replication and host defense.[9] Anti-viral therapeutic drugs which also reduce inflammation seem to be the most effective treatment, but research is still ongoing.[12]Reactive oxygen species are upregulated during inflammation as part of the immune response to defend against pathogens.[13] However, excessive inflammation causes dangerous levels of reactive oxygen species which cause oxidative stress to tissues.[13] The immune system naturally produces antioxidant compounds to regulate and detoxify reactive oxygen species.[13] Anti-oxidative therapy with supplements such as vitamin C, vitamin E, curcumin, or baicalin is speculated to reduce infection severity in COVID-19,[14][12] but previous research has not found antioxidants supplementation to be effective in the prevention of other diseases.[15] Shifting from the typical western diet to a Mediterranean diet or plant-based diet may improve COVID-19 health outcomes by reducing prevalence of comorbidities (i.e. obesity or hypertension), decreasing intake of pro-inflammatory foods, and increasing consumption of anti-inflammatory and antioxidant nutrients.[12][16][17]
Research
While systemic inflammation may be induced by multiple external factors, research suggests that a lack of control by tolerogenic dendritic cells and T-regulatory cells (Treg) is possibly the primary risk factor. In functioning immune responses, T-helper and T-cytotoxic cells are activated by presentation of antigens by antigen-presenting cells (APCs). Chief among these are dendritic cells (DCs). When a DC presents an antigen to a Treg cell, a signal is then sent to the nucleus of the DC, resulting in the production of indoleamine 2,3-dioxygenase (IDO). IDO inhibits T cell responses by depleting tryptophan and producing kynurenine, which is toxic to the cell.[citation needed]
Individuals susceptible to developing chronic systemic inflammation appear to lack proper functioning of Treg cells and TDCs. In these individuals, a lack of control of inflammatory processes results in multiple chemical and food intolerances, and autoimmune diseases.[citation needed]
↑ Katsiki, Niki; Manes, Christos (February 2009). "Is there a role for supplemented antioxidants in the prevention of atherosclerosis?". Clinical Nutrition (Edinburgh, Scotland). 28 (1): 3–9. doi:10.1016/j.clnu.2008.10.011. ISSN1532-1983. PMID19042058.
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