Live Biotherapeutics Drug Discovery Service for COPD
Overview
Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease, characterized by incomplete reversible chronic inflammation and significant airflow obstruction. It is also a preventable and treatable respiratory disease and is one of the major causes of global incidence rate and mortality. Smoking is the primary risk factor for COPD and has been shown in clinical and preclinical studies to alter the gut microbiota. An increasing number of studies indicate that the latest advances in genomics and metabolomics reveal the role of gut microbiota and its metabolites in COPD. Dysfunction of gut microbiota is considered an important component of COPD pathophysiology, and gut microbiota and related metabolites may affect the occurrence and development of COPD by regulating immunity and inflammation.
Fig.1 Microbiota-gut-lung axis.1
Lung and Gut Microbiota in COPD
COPD is associated with the imbalance of lung flora and the overgrowth of pathogenic bacteria, which leads to the accelerated decline of lung function. Lung microbiota plays a key role in the occurrence and development of COPD. Clinical research has demonstrated that cigarette smoking, considered as one of the factors involved in the pathogenesis of COPD, also decreases the range of the gut microbes, and this development, in turn, is also involved in the pathogenesis of COPD.
New Therapeutic Approaches for the Management of COPD
The treatment of COPD is mainly based on symptomatic treatment, and no drug can fundamentally cure COPD without side effects. At present, the treatment of COPD includes both pharmacological and non-pharmacological strategies. There is an urgent need to elucidate the pathogenesis of COPD and explore new treatment options, and the homeostasis of gut microbiota is one of the potential considerations for the prevention or treatment of COPD.
In COPD mice, probiotic treatment alleviated cell density in BALF and restored the balance between cytokines and chemokines, thereby reducing alveolar enlargement and collagen deposition. Thus, the probiotic treatment produced positive results in COPD mice, indicating its potential therapeutic value for the disease.
In the smoke-based models, fecal transplantation can improve gut microbiota imbalance, suggesting that gut microbiota may play a causal role in the pathogenesis of COPD. Especially Parabacteriodies goldsteinii (P. goldsteinii), which partially inhibits the toll-like receptor 4 (TLR4) signaling pathway through lipopolysaccharide, reduces intestinal inflammation, enhances colon mitochondrial function and ribosomal activity, restores serum amino acid metabolism, and inhibits lung infection. Therefore, this strain or its derived lipopolysaccharides can serve as a new drug for treating COPD.
Evs have the potential to mediate the delivery of therapeutic molecules without causing adverse immune reactions. Therefore, EVs produced by probiotics may play a positive role in stabilizing the dysbiosis of the lung microenvironment and further improve the therapeutic effect. Probiotic-derived EVs are a novel treatment for drug-resistant pathogens.
Our Probiotic Services for COPD Research
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Research Articles
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Available Services
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Oral feeding with probiotic Lactobacillus rhamnosus attenuates cigarette smoke-induced COPD in C57Bl/6 mice: Relevance to inflammatory markers in human bronchial epithelial cells.2
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Creative Biolabs has accumulated a lot of project experience in the field of probiotics, including laboratory-scale preparation of probiotics, probiotics treatment, and other subsequent analyses. If you are conducting relevant research on probiotics and COPD, you may wish to contact us, perhaps we can provide you with more reasonable solutions and fully acceptable quotes.
References
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Varela-Trinidad, Gael Urait, et al. "Probiotics: Protecting our health from the gut." Microorganisms 10.7 (2022): 1428.
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Carvalho, J. L., et al. "Oral feeding with probiotic Lactobacillus rhamnosus attenuates cigarette smoke-induced COPD in C57Bl/6 mice: Relevance to inflammatory markers in human bronchial epithelial cells." PLoS One 15.4 (2020): e0225560.
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Distributed Under Open Access license CC BY 4.0, without modification.
For Research Use Only. Not intended for use in food manufacturing or medical procedures (diagnostics or therapeutics). Do Not Use in Humans.
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