The word inflammation originates from the Latin word “inflammare” which translates to “set on fire”. In accordance with this, our body responds to various kinds of intrinsic or extrinsic injuries by setting itself on fire, locally or systemically, to rescue itself from prolonged tissue damage and to initiate the process of healing. However, decades of research 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. Intriguingly, 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, Human Immunodeficiency Virus (HIV), and Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), which recently affected millions of people worldwide, by influencing pathological inflammation at a genetic level.
In addition to the genetic factors, inflammation can also be triggered by multiple non-genetic factors including microbiome, toxic compounds, diet, and stress, which affects the epigenome and secretome of tissue microenvironment. Altogether, these genetic and non-genetic associations 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.
In this research topic, we welcome the submission of original articles, reviews, and perspectives related to, but not limited to,
a) The understanding of mechanisms of inflammation and inflammatory responses in a variety of diseases.
b) Molecular and computational methodologies to identify new genetic variants linked to the cause and consequences of inflammatory diseases.
c) Novel OMICS approaches to identify targets of translational and pathological inflammation.
The word inflammation originates from the Latin word “inflammare” which translates to “set on fire”. In accordance with this, our body responds to various kinds of intrinsic or extrinsic injuries by setting itself on fire, locally or systemically, to rescue itself from prolonged tissue damage and to initiate the process of healing. However, decades of research 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. Intriguingly, 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, Human Immunodeficiency Virus (HIV), and Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), which recently affected millions of people worldwide, by influencing pathological inflammation at a genetic level.
In addition to the genetic factors, inflammation can also be triggered by multiple non-genetic factors including microbiome, toxic compounds, diet, and stress, which affects the epigenome and secretome of tissue microenvironment. Altogether, these genetic and non-genetic associations 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.
In this research topic, we welcome the submission of original articles, reviews, and perspectives related to, but not limited to,
a) The understanding of mechanisms of inflammation and inflammatory responses in a variety of diseases.
b) Molecular and computational methodologies to identify new genetic variants linked to the cause and consequences of inflammatory diseases.
c) Novel OMICS approaches to identify targets of translational and pathological inflammation.
