Fine particulate matter (PM2.5) have become a major public health concern because of their adverse effects on health. Lungs are considered the primary organ affected by PM2.5. In order to understand the mechanism underlying PM2.5-induced lung injury, 16S rRNA gene sequencing, and liquid chromatography-mass spectrometry (LC-MS) metabolomics analysis were conducted to investigate the impact of PM2.5 exposure on lung microbiome and its metabolic profile. Mice were exposed to PM2.5 through intratracheal instillation and a lung injury model was established. 16S rRNA gene sequencing indicated that PM2.5 exposure significantly altered the richness, evenness, and composition of the lung microbiome. Metabolomics profiling showed that the levels of lung metabolites were perturbed after PM2.5 exposure. The altered metabolites mainly belonged to metabolic pathways, such as the citrate cycle, glyoxylate and dicarboxylate metabolism, pyruvate metabolism, purine and pyrimidine metabolism, and valine, leucine, and isoleucine metabolism. The altered lung microbiota showed significant correlations with lung metabolites. The levels of fumaric acid negatively correlated with the relative abundance of Ruminococcaceae, Enterobacteriaceae, and Pseudomonadaceae. These results revealed that PM2.5 exposure not only significantly altered the lung microbiome composition but also perturbed a number of metabolites involved in diverse metabolic pathways. This study improves our understanding of the mechanism of lung injury after PM2.5 exposure.

Early life represents a critical period for the development and growth of the lungs. Adverse exposures in this stage may drive the development of chronic obstructive pulmonary disease (COPD). Thus, we quantitatively evaluated the impact of different early life exposures on COPD in adulthood. The PubMed, Embase and Cochrane Library electronic databases were searched for articles published from January 2001 to October 2020. A total of 30 studies (795,935 participants) met the criteria and were included in the review. We found a significant association of COPD with childhood serious respiratory infections, pneumonia or bronchitis (pooled adjusted OR [aOR], 2.23 [95% CI, 1.63–3.07]). The probability of COPD was increased 3.45‐fold for children with than without asthma (pooled aOR, 3.45 [95% CI, 2.37–5.02]). In addition, the probability of COPD was associated with maternal smoking (pooled aOR, 1.42 [95% CI, 1.17–1.72]), any child maltreatment (pooled aOR, 1.30 [95% CI, 1.18–1.42]) and low birth weight (pooled aOR, 1.58 [95% CI, 1.08–2.32]) but not childhood environmental tobacco smoke exposure (pooled aOR, 1.15 [0.83–1.61]) or premature birth (pooled aOR, 1.17 [95% CI, 0.87–1.58]). Furthermore, subgroup analyses revealed that probability was increased for only women with childhood physical abuse, sexual abuse and exposure to intimate partner violence. Factors resulting in COPD in adults could trace back to early life. Childhood respiratory disease, maltreatment, maternal smoking and low birth weight increase the risk of COPD. Promising advances in prevention strategies for early life exposures could markedly decrease the risk of COPD.

Background: Oxidative stress is associated with outcomes of chronic lung disease. The oxidative stress-related exposures of diet and lifestyle can be evaluated by the oxidative balance score (OBS), and higher OBS scores indicate more significant antioxidant exposures. But the relationship between OBS and lung health is unknown.Purpose: The aim of this study was to explore the association between OBS and lung health (respiratory symptoms, chronic lung disease, and lung function).Methods: A series of models, including weighted linear models, weighted logistic regression, and weighted multinomial logistic regression, were performed to assess the associations of OBS with respiratory symptoms, chronic lung disease, and lung function. The models adjusted by age, race/ethnicity, gender, educational background, poverty-to-income ratio, and dietary energy were also performed.Results: Cross-sectional data of 5,214 participants from the National Health and Nutrition Examination Survey for the years 2007–2012 were analyzed. For every one-unit increase in OBS, the odds of wheezing/chronic bronchitis decreased by 6%. Increased OBS was associated with higher percent-predicted forced expiratory volume in one second (FEV1) (adjusted mean difference (MD), 0.21%; 95% CI: 0.10–0.32) and percent-predicted forced vital capacity (FVC) (adjusted MD, 0.15%; 95% CI: 0.07–0.24). A significantly lower risk of wheezing/chronic bronchitis was found in participants in the second/third/fourth OBS quartile compared to those in the first OBS quartile (all P for trend < 0.05). Moreover, higher percent-predicted FEV1 and FVC were also found in the third quartile and fourth quartile (all P for trend < 0.05). Furthermore, both dietary and lifestyle components were tightly related to pulmonary outcomes. Many associations were maintained after stratified by sex or after sensitivity analyses.Conclusion: Oxidative balance score was negatively correlated with the diagnosis of chronic bronchitis/wheezing/restrictive spirometry pattern and positively correlated with percent-predicted FVC and FEV1. It seems that the higher the OBS score, the better the pulmonary outcomes. The findings highlight the importance of adherence to an antioxidant diet and lifestyle and that it contributes to lung health.

Background: Fibrosis is often associated with aberrant repair mechanisms that ultimately lead to organ failure. In the lung, idiopathic pulmonary fibrosis (IPF) is a fatal form of interstitial lung disease for which there is currently no curative therapy. From the cell biology point of view, the cell of origin and eventual fate of activated myofibroblasts (aMYFs) have taken centre stage, as these cells are believed to drive structural remodelling and lung function impairment. While aMYFs are now widely believed to originate from alveolar fibroblasts, the heterogeneity and ultimate fate of aMYFs during fibrosis resolution remain elusive. We have shown previously that aMYF dedifferentiation and acquisition of a lipofibroblast (LIF)-like phenotype represent a route of fibrosis resolution.Methods: In this study, we combined genetic lineage tracing and single-cell transcriptomics in mice, and data mining of human IPF datasets to decipher the heterogeneity of aMYFs and investigate differentiation trajectories during fibrosis resolution. Furthermore, organoid cultures were utilised as a functional readout for the alveolar mesenchymal niche activity during various phases of injury and repair in mice.Results: Our data demonstrate that aMYFs consist of four subclusters displaying unique pro-alveologenicversuspro-fibrotic profiles. Alveolar fibroblasts displaying a high LIF-like signature largely constitute both the origin and fate of aMYFs during fibrogenesis and resolution, respectively. The heterogeneity of aMYFs is conserved in humans and a significant proportion of human aMYFs displays a high LIF signature.Conclusion: Our work identifies a subcluster of aMYFs that is potentially relevant for future management of IPF.

Background: The muscle quality index (MQI), as an important component of sarcopenia, is defined as the ratio of muscle strength to muscle mass. Lung function, is a clinical indicator to assess ventilation and air exchange function. This study investigated the relationship between lung function indices and MQI in the NHANES database from 2011 to 2012.Methods: This study included 1,558 adults from the National Health and Nutrition Examination Survey from 2011 to 2012. Muscle mass and muscle strength were assessed using DXA and handgrip strength, and all participants underwent pulmonary function measurements. Multiple linear regression and multivariable logistic regression were used to assess the correlation between the MQI and lung function indices.Results: In the adjusted model, MQI was significantly correlated with FVC% and PEF%. And, after quartiles of MQI in Q3, where FEV₁%, FVC%, and PEF% were all associated with MQI, in Q4, a lower relative risk of a restrictive spirometry pattern was linked to increased MQI. Compared to the lower age group, the relationship between the MQI and lung function indices was more significant in the higher age group.Conclusion: There was an association between the MQI and lung function indices. Furthermore, in the middle-aged and older adult populations, lung function indicators and restrictive ventilation impairment were significantly associated with MQI. This implies that improving lung function through muscle training may be beneficial to this group.