Genetic and Non-Genetic Inflammation Networks in Major Human Diseases

Created 11 Apr 2023| Updated 30 Apr 2024 | 5 articles
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Inflammation is an adaptive response and integral part of animal biology against a myriad of factors including infection, trauma, and disease. Considerable progress has been made in understanding the cellular and molecular events that are involved in the acute inflammatory response to infection and, to a lesser extent, tissue injury and chronic inflammation.

Numerous studies have shown how the clinical manifestation of inflammation can also be pathological and prime the tissue niche for the progression of myriad complex diseases such as cancer, microbial resistance, autoimmune disorders, and gut microbiota dysbiosis.

Interestingly, several genome-wide association studies (GWAS), whole-exome sequencing (WES), and single cell-based technologies have highlighted how rare genetic mutations or variations modulate the susceptibility of an individual to infectious pathogens, such as Mycobacterium tuberculosis (TB), Human Immunodeficiency Virus (HIV), and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), by influencing pathological inflammation at a genetic level.

In addition to the genetic determinants, inflammation can also be triggered by multiple non-genetic factors including the microbiome, toxic compounds, diet, and stress, which affect the epigenome and secretome of the tissue microenvironment.

Altogether, these genetic and non-genetic networks in inflammatory diseases have long been established in several clinical and epidemiological studies. However, we still lack a significant understanding of causal links and strategic explanations for the interaction between genome, epigenome, microbiome, metabolome, and inflammatome. Therefore, we need a cohesive approach focusing on both genetic and non-genetic determinants to curb pathological inflammation.

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Originally published in Journal of Inflammation Research, Volume: 16 (31 Dec 2023)

Published online: 22 Feb 2023
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