Changes In Lung Microbiome Research Articles

Pathogenesis of Tobacco-Associated Lung Adenocarcinoma Is Closely Coupled with Changes in the Gut and Lung Microbiomes.

Microbial dysbiosis has emerged as a modulator of oncogenesis and response to therapy, particularly in lung cancer. Here, we investigate the evolution of the gut and lung microbiomes following exposure to a tobacco carcinogen. We performed 16S rRNA-Seq of fecal and lung samples collected prior to and at several timepoints following (nicotine-specific nitrosamine ketone/NNK) exposure in Gprc5a−/− mice that were previously shown to exhibit accelerated lung adenocarcinoma (LUAD) development following NNK exposure. We found significant progressive changes in human-relevant gut and lung microbiome members (e.g., Odoribacter, Alistipes, Akkermansia, and Ruminococus) that are closely associated with the phenotypic development of LUAD and immunotherapeutic response in human lung cancer patients. These changes were associated with decreased short-chain fatty acids (propionic acid and butyric acid) following exposure to NNK. We next sought to study the impact of Lcn2 expression, a bacterial growth inhibitor, given our previous findings on its protective role in LUAD development. Indeed, we found that the loss of Lcn2 was associated with widespread gut and lung microbiome changes at all timepoints, distinct from those observed in our Gprc5a−/− mouse model, including a decrease in abundance and diversity. Our overall findings apprise novel cues implicating microbial phenotypes in the development of tobacco-associated LUAD.

Exposure to particulate matter 2.5 leading to lung microbiome disorder and the alleviation effect of Auricularia auricular-judae polysaccharide.

The aim of the paper is to explore the role of lung microbiome disorder in lung tissue injury induced by exposure to particulate matter with a maximum diameter of 2.5 μm (PM2.5) and the alleviation effect of Auricularia auricular-judae polysaccharide (AAP). Sprague Dawley rats were given PM2.5 suspension at a dose of 20 mg/l twice a week for 8 weeks. Then, 100 mg/kg or 200 mg/kg of AAP was administered to the rats after PM2.5 exposure. The bronchoalveolar lavage fluid (BALF) and lung tissue samples were collected at the end of the experiment. The BALF was meant to detect changes in lung microbiome by 16S sequences and cluster analysis, with the application of the principal component analysis and the partial least squares discriminant analysis. The levels of interferon-γ (IFN-γ), and interleukin (IL)-4, IL-8, and IL-10 in lung tissue were detected by the enzyme-linked immunosorbent assay method. The pathological changes in lung tissue were observed by hematoxylin and eosin staining. After PM2.5 exposure, the alveolar septum was widened, and the structures of alveolar walls were destroyed. There was inflammatory cells infiltration in the alveolar space and the interstitial space. Alpha diversity in BALF showed that the Chao1, ACE, Simpson, and Shannon values were increased, and the lung microbiome analysis revealed that the relative abundance of Firmicutes and Clostridium increased, while the relative abundance of Bacteroidetes and Akkermansia decreased. The contents of IFN-γ and IL-8 in lung tissue increased while the content of IL-10 decreased. After the administration of AAP, the alveolar structure damage was alleviated, and the interstitial hemorrhage, edema, and inflammatory cells infiltration were reduced. The Chao1 and ACE values decreased, and the taxonomic abundance values of Akkermansia were much higher. Simultaneously, the contents of IFN-γ, IL-4, and IL-8 decreased, and the content of IL-10 increased. It was found that PM2.5 resulted in lung microbiome disorder, which might lead to the inflammation of lung tissue. It was also revealed that AAP could alleviate the inflammatory damage of lung tissue induced by PM2.5. Int J Occup Med Environ Health. 2022;35(6):651-64.

The pulmonary microbiome: recent advances in understanding its role in chronic lung allograft dysfunction.

Lung transplantation presents a rescue therapy for those with end-stage lung disease. Survival in lung transplant patients remains limited due to chronic lung allograft dysfunction (CLAD), a range of pathologic manifestations leading to graft loss. The mechanisms underlying CLAD remain poorly understood, and the lung microbiome has been suggested as a potential contributor to this condition. This review aims to explore how the pulmonary microbiome is impacted by lung transplantation, and how alterations in this microbiome may contribute to the pathogenesis of CLAD. The pulmonary microbiome is made up of a range of microorganisms, and it varies considerably in lung transplant patients when compared with healthy controls. The lung microbiome changes over the early transplant period, and the composition of species appears to have an impact on inflammatory responses within the lungs. A number of studies have shown that an increase in bacterial biomass in the allograft, and enrichment with the genera Proteobacteria, or more specifically, Pseudomonas species, is associated with CLAD. This area of research is still in its infancy; however, the suggestion that changes in the composition of the microbiome and enrichment with certain species may predispose to the pathologic changes that underlie CLAD indicate that modulation of the microbiome may be of use in potential future therapeutics.

Lung microbiome mediates the progression from chronic obstructive pulmonary disease to lung cancer through inflammation.

Lung microbiome exists in the respiratory tract and parenchymal tissues. It mediates lung injury through a variety of mechanisms, including bacterial disturbance, metabolites, inflammatory response, immune response, and genotoxicity. Accumulating evidences suggest that changes in lung microbiome correlates with chronic obstructive pulmonary disease (COPD) and lung cancer, and the microbiome promotes the progression from COPD to lung cancer. In this review, we mainly introduce the impairment of the homeostasis of the lung microbiome and its inflammation that leads to COPD and lung cancer, then focus on how the microbiome mediates the progression from COPD to lung cancer through inflammatory response. The review may provide a new theoretical basis for clinical prevention, optimal treatment strategy and design of new drugs for COPD and lung cancer.

Potential health impacts and lung microbiome changes among smoking and smokeless tobacco use : A technical scan

Globally, 1.3 billion peoples use tobacco products daily, most of them from low- and middle-income countries. Every year, 8 million of the population died because of the usage of tobacco, as per the WHO report. Tobacco-related diseases, likely lung cancer, emphysema chronic obstructive pulmonary disease, and chronic respiratory diseases, are more common. Nicotine is a highly addictive chemical found in the tobacco plant and also in all other tobacco products. All tobacco products contain nicotine that causes the release of dopamine in the pleasure and motivation areas of the brain. Both smoking and smokeless tobacco products contain many harmful chemicals that affect the lung mucociliary clearance and also inactivate the immune system and lead to increases in the risk of infection and the development of deleterious bacterial growth in the lungs. In the lung microbiome, Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and Pseudomonas aeruginosa bacterial species were found to a higher level in smoking tobacco users as that may increase morbidity and mortality. The lung microbiome changes taking place in the lung due to smokeless tobacco usage are less documented so far. In future research, microbiome studies help to understand disease pathogenesis.

Microbiome in Chronic Obstructive Pulmonary Disease: Role of Natural Products Against Microbial Pathogens.

The "microbiome" is the operative term to refer to a collection of all taxa constituting microbial communities, such as bacteria, archaea, fungi and protists (originally microbiota). The microbiome consists of the indigenous microbial communities and of the host environment that they inhabit. Actually, it has been shown that there is a close relationship between the microbiome and human health and disease condition. Although, initially, the lung was considered sterile, actually, the existence of a healthy lung microbiome is usually accepted. Lung microbiome changes are reported in Chronic Obstructive Pulmonary Disease (COPD) and in its exacerbation. Viral and bacterial infections of the respiratory system are a major cause of COPD exacerbations (AECOPD) leading to increased local and systemic inflammation. Detection rates of virus in AECOPD are variable between 25-62% according to the detection method. The study of human airway and lung disease virome is quite recent and still very limited. The purpose of this review is to summarize recent findings on the lung microbiome composition with a special emphasis on virome in COPD and in AECOPD. Some drugs of natural origins active against resistant bacteria and virus are described.

P207 Start of lumacaftor/ivacaftor in adult cystic fibrosis patients with homozygous F508del results in temporal and moderate changes in lung microbiome and metabolome

P207 Start of lumacaftor/ivacaftor in adult cystic fibrosis patients with homozygous F508del results in temporal and moderate changes in lung microbiome and metabolome

497 - The Oropharynx Rather than the Stomach is the Primary Driver of Lung Microbiome Changes in Aspirating Children

497 - The Oropharynx Rather than the Stomach is the Primary Driver of Lung Microbiome Changes in Aspirating Children

The lung microbiome and exacerbations of COPD.

Traditional culture methods have identified airway bacterial pathogens that cause acute exacerbations of chronic obstructive pulmonary disease (COPD), and contribute to airway inflammation and COPD progression. However, conventional microbiology is limited by low sensitivity and bias toward predetermined and predominant pathogens. Highly sensitive, unbiased microbiome techniques overcome these limitations. Here, we present recent lung microbiome data, specifically in the context of smoking, COPD, and exacerbations. In contrast to the sterile lung environment found with conventional microbiology, microbiome techniques demonstrate a lower respiratory tract microbiome in health. Alterations in the lung microbiome with smoking and COPD have been clearly demonstrated by culture techniques, however, the findings in microbiome studies are limited and controversial. Increasing COPD disease severity is associated with a reduction in microbial diversity. Though microbial community structure does not change with exacerbation, there are notable changes in its composition. Antibiotic and corticosteroid treatment of acute exacerbations of COPD have significant but opposing effects on microbiome composition. The composition of the lung microbiome changes with smoking, the severity of COPD, during acute exacerbations and with the use of steroids and/or antibiotics. Understanding the role of the microbiome in disease progression and development of exacerbations will lead to novel therapies.

The Murine Lung Microbiome Changes During Lung Inflammation and Intranasal Vancomycin Treatment.

Most microbiome research related to airway diseases has focused on the gut microbiome. This is despite advances in culture independent microbial identification techniques revealing that even healthy lungs possess a unique dynamic microbiome. This conceptual change raises the question; if lung diseases could be causally linked to local dysbiosis of the local lung microbiota. Here, we manipulate the murine lung and gut microbiome, in order to show that the lung microbiota can be changed experimentally. We have used four different approaches: lung inflammation by exposure to carbon nano-tube particles, oral probiotics and oral or intranasal exposure to the antibiotic vancomycin. Bacterial DNA was extracted from broncho-alveolar and nasal lavage fluids, caecum samples and compared by DGGE. Our results show that: the lung microbiota is sex dependent and not just a reflection of the gut microbiota, and that induced inflammation can change lung microbiota. This change is not transferred to offspring. Oral probiotics in adult mice do not change lung microbiome detectible by DGGE. Nasal vancomycin can change the lung microbiome preferentially, while oral exposure does not. These observations should be considered in future studies of the causal relationship between lung microbiota and lung diseases.