Abstract
The microbiome plays a fundamental role in how the immune system develops and how inflammatory responses are shaped and regulated. The “gut-lung axis” is a relatively new term that highlights a crucial biological crosstalk between the intestinal microbiome and lung. A growing body of literature suggests that dysbiosis, perturbation of the gut microbiome, is a driving force behind the development, and severity of allergic asthma. Animal models have given researchers new insights into how gut microbe-derived components and metabolites, such as short-chain fatty acids (SCFAs), influence the development of asthma. While the full understanding of how SCFAs influence allergic airway disease remains obscure, a recurring theme of epigenetic regulation of gene expression in several immune cell compartments is emerging. This review will address our current understanding of how SCFAs, and specifically butyrate, orchestrates cell behavior, and epigenetic changes and will provide a detailed overview of the effects of these modifications on immune cells in the context of allergic airway disease.
Highlights
The gut microbiome is an intricate community composed of microorganisms from diverse groups of bacteria, fungi, protists, archaea, and viruses
Decades of research have revealed the significance of the gut microbiome in physiological processes, initially in regulating nutrition and metabolism [1] and, more recently, in the pathogenesis of respiratory, gastrointestinal, and neurological disease [2,3,4,5,6,7]
We have found that both, the vancomycin-induced severe airway disease (AAD), and the restorative effects of Short-chain fatty acids (SCFAs)-supplementation require early life application to alter the subsequent adult allergic responses
Summary
The gut microbiome is an intricate community composed of microorganisms from diverse groups of bacteria, fungi, protists, archaea, and viruses. The highest levels of SCFAs are found in the proximal colon, where they are either consumed locally as an energy source by intestinal epithelial cells (colonocytes) or transported across the gut epithelium and absorbed into the bloodstream [9, 10]. Especially butter, contain butyrate but these sources of the metabolite are paltry compared to the butyrate produced by intestinal commensal bacteria from non-digestible dietary fiber [11]. In humans, this fermentation primarily takes place in the proximal large intestine by butyrate-producing Firmicutes phylum, including Ruminococcaceae, Lachnospiraceaes, Erysipelotrichaeceae and Clostridiaceae [reviewed in [11]]. Evidence for the effect of butyrate on inflammatory disease pathophysiology outside of the liver and intestine is mounting
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