Preventive and Therapeutic Adjunctive Roles of Immune Optimization on Inflammatory and Infectious Diseases: A Mini Review
Abstract
INTRODUCTIONThe cardiovascular disease spectrum contains inflammatory and infective heart diseases (IIHDs), which manifest as pericarditis, myocarditis, and endocarditis. Inflammatory heart diseases are autoimmune or auto-inflammatory and have similar causative non-infective factors like immuno-toxic lifestyle habits, air pollutants, etc. Inflammatory immune dysfunction underlines the pathogenesis of inflammatory heart diseases.[1] Viruses are the main infective causative agents of pericarditis and endocarditis, while myocarditis is caused by bacteria. Genetic predisposition may explain rare heart inflammation in young people.[2]
The immune system in health and disease may be enhanced by immune optimization (IO) and dysfunction, respectively. An optimized immune system dissuades inflammatory and infective disease processes. Immune dysfunction enhanced by toxin/infectious agents may reflect a spectrum of IIHDs that share similar immune dysfunctional pathogenesis. Inflammatory cytokines play pivotal roles in the disease processes. The biology and correlation of inflammatory cytokines (IL-6, IL-1, IL-33, TNF-alpha, IL-10, and IL-8) concerning IIHDs is well known.[3] However, the actual inflammatory dysfunctional disease mechanisms are unknown.
Inflammatory heart diseases have autoimmune and auto-inflammatory etiology.[1] They share similar inflammatory pathways with dysfunctional T cells playing central roles in their immunopathogenesis. Transendothelial migration of T cells is mediated by cellular adhesion molecules (CAMs), which are regulated by pro-inflammatory cytokines produced by T cells in immunological processes.[4] Viruses bind to CAMs to gain entry to the host cell. Bacterial surface proteins are frequently recognized and bound to by CAMs.[5,6] In contrast to jet lesions, which predispose heart valve colonization by bacteria, infection of non-bacterial thrombotic vegetation requires a predisposition that is partially operative amidst T cell dysfunctional activities.[7]
The combined incidence of inflammatory and infectious diseases, which affects all systems of the body, is alarming and should be a dire public health concern. Furthermore, their rising incidence, morbidity, and mortality underscore the limitations of current drug treatment modalities. Moreover, these drugs are not without side effects. Immune optimization (IO) interventions with immune optimizers such as a good diet, adequate sleep, and moderate intensity should be alluring preventive and adjunctive therapeutic strategies to mitigate immune dysfunction—a forerunner to inflammatory and infectious diseases. Hence, this review aims to highlight IO as a preventive and therapeutic adjunct for the management of inflammatory and infectious diseases. Additionally, discussing a putative T cell immune dysfunction model of inflammatory and infectious diseases using inflammatory and infective heart diseases as classic examples should pave the way for a better understanding of the preventive and therapeutic adjunctive roles of immune optimization for the management of inflammatory and infectious diseases.
MATERIALS AND METHODSOnline searches were conducted on databases such as Google Scholar, PubMed, Biomed Central, and SciELO. Articles were reviewed using keywords such as Immune optimization/dysfunction, T lymphocyte activation/dysfunction, inflammatory cytokines, disease prevention, and therapeutic adjunct.
RESULTSOf the 314 articles identified from databases, 41 were duplicates and 13 not related to the review topic were excluded. Of the 260 articles assessed for legibility, 16 articles were included in the Mini review [Figure 1].
PRISMA flow diagram for the Mini review detailing the database searches and the number of articles screened