Association of Intestinal Microbial Dysbiosis With Chronic Obstructive Pulmonary Disease

Abstract

Normal gut flora plays various beneficial roles for the human body, including the protection against inflammatory states and mucosal viral infections. It also influences the immune system of the body. The metabolites produced by the gut bacteria control local and other systemic organs' immune functions like the lungs and brain, playing a role in their response to acute and chronic illnesses. Probiotics have shown beneficial effects on lung health. On the contrary, dysbiosis is associated with several diseases, including asthma, chronic bronchitis, emphysema, allergies, and other acute viral infections. By altering the diet of patients with respiratory diseases like patients with chronic obstructive pulmonary diseases (COPD), we may be able to mitigate their conditions. This literature review aims to discuss the mechanisms altering the gastrointestinal flora, the pathophysiology of gut and lung axis, the role of diet in gut microbe health, and the association of COPD with gut dysbiosis and peptic ulcer disease (PUD). We have extracted the data from PubMed and Google Scholar, consisting of review articles, case-control studies, and animal studies. The studies showed an association between gut microbes and different lung diseases. It is found that gut dysbiosis not only disrupts intestinal immunity but may also facilitate the development of COPD. Present studies also show an increased seroprevalence of Helicobacter pylori in patients with COPD. The strategies that can improve lung functions, especially in COPD patients, include prebiotics and probiotic supplementation to a diet more balanced than the current average American diet.

Keywords: association of copd with pud; copd; gut dysbiosis; gut-lung axis; mucosal immunity; pathophysiology of copd.

Figure 1. The gut-lung axis

A model showing the gut-lung axis and the gut microbiota's regulatory impact on lung function immune reaction by priming DCs and then proliferation and activation of T-cells in response to antigens. Gut dysbiosis results in impaired T-cell proliferation and activation, thus causing a reduction in lung immune reaction DCs, dendritic cells; SCFA, short-chain fatty acids; LPS, lipopolysaccharides

Figure 2. Representation of the interaction between the lungs and the intestine in disease settings.

Microbial dysbiosis within the intestine results in exaggerated immune reactions to the microbiome, as well which may lead to loss of integrity and function of epithelial barrier in both the intestines and the lungs COPD, chronic obstructive pulmonary disease; IL-1, interleukin 1; TNF, tumor necrosis factor; IgG, immunoglobulin G; IFN, interferon