Abstract

Inflammatory bowel disease (IBD) and chronic obstructive pulmonary disease (COPD) are chronic inflammatory diseases of the gastrointestinal and respiratory tracts, respectively. These mucosal tissues bear commonalities in embryology, structure and physiology. Inherent similarities in immune responses at the two sites, as well as overlapping environmental risk factors, help to explain the increase in prevalence of IBD amongst COPD patients. Over the past decade, a tremendous amount of research has been conducted to define the microbiological makeup of the intestine, known as the intestinal microbiota, and determine its contribution to health and disease. Intestinal microbial dysbiosis is now known to be associated with IBD where it impacts upon intestinal epithelial barrier integrity and leads to augmented immune responses and the perpetuation of chronic inflammation. While much less is known about the lung microbiota, like the intestine, it has its own distinct, diverse microflora, with dysbiosis being reported in respiratory disease settings such as COPD. Recent research has begun to delineate the interaction or crosstalk between the lung and the intestine and how this may influence, or be influenced by, the microbiota. It is now known that microbial products and metabolites can be transferred from the intestine to the lung via the bloodstream, providing a mechanism for communication. While recent studies indicate that intestinal microbiota can influence respiratory health, intestinal dysbiosis in COPD has not yet been described although it is anticipated since factors that lead to dysbiosis are similarly associated with COPD. This review will focus on the gut-lung axis in the context of IBD and COPD, highlighting the role of environmental and genetic factors and the impact of microbial dysbiosis on chronic inflammation in the intestinal tract and lung.

Highlights

  • Inflammatory bowel disease (IBD) and chronic obstructive pulmonary disease (COPD) are chronic inflammatory diseases that affect the gastrointestinal tract and respiratory system, respectively, with both being characterized by recurrent disease cycles that result in tissue damage and worsening of disease symptoms

  • While these data suggest that inflammation is sufficient to induce dysbiosis, it is clear that genetic susceptibility plays a role since T. gondii induced heightened dysbiosis and Adherent-invasive Escherichia coli (AIEC) invasion in mice lacking the ileitis susceptibility gene nucleotidebinding oligomerization domain-containing protein 2 (NOD2), while disease was significantly muted in mice lacking the proinflammatory CC chemokine receptor 2 (CCR2), which are a model of ileitis resistance [58]

  • Microbial dysbiosis has a pivotal role in the development of IBD and COPD impacting on the intestinal and respiratory epithelial barriers and promoting damaging immune responses

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Summary

INTRODUCTION

Inflammatory bowel disease (IBD) and chronic obstructive pulmonary disease (COPD) are chronic inflammatory diseases that affect the gastrointestinal tract and respiratory system, respectively, with both being characterized by recurrent disease cycles that result in tissue damage and worsening of disease symptoms. The gastrointestinal and respiratory tracts share structural similarities which may result in part from common embryonic origin in the primitive foregut [1]. Its hypothesized that these structural similarities may account for inherent parallels in the immune responses at these two sites and contribute to the dynamic involvement of the gut-lung axis in inflammation

Inflammatory Bowel Disease
Chronic Obstructive Pulmonary Disease
Linking IBD and COPD
Healthy Intestinal Microbiota
Healthy Lung Microbiota
Dysbiosis of Intestinal Microbiota in IBD
Genetics of IBD and Its Role in Intestinal
Lung Dysbiosis Is Observed in COPD
FACTORS LINKING IBD AND COPD
Dietary Fat Can Alter the Gut Microbiota and Influence Disease
Have Therapeutic Benefits in CD and COPD
INTESTINAL MICROBIOTA
Disease Exacerbations
Treatment Strategy
Findings
CONCLUSION

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