Idiopathic pulmonary fibrosis (IPF) is a chronic disease mainly associated with aging and, to date, its causes are still largely unknown. It has been shown that dietary habits can accelerate or delay the occurrence of aging-related diseases; however, their potential role in IPF development has been underestimated so far. The present review summarizes the evidence regarding the relationship between diet and IPF in humans, and in animal models of pulmonary fibrosis, in which we discuss the bioactivity of specific dietary food ingredients, including fatty acids, peptides, amino acids, carbohydrates, vitamins, minerals and phytochemicals. Interestingly, many animal studies reveal preventive and therapeutic effects of particular compounds. Furthermore, it has been recently suggested that the lung and gut microbiota could be involved in IPF, a relationship which may be linked to changes in immunological and inflammatory factors. Thus, all the evidence so far puts forward the idea that the gut-lung axis could be modulated by dietary factors, which in turn have an influence on IPF development. Overall, the data reviewed here support the notion of identifying food ingredients with potential benefits in IPF, with the ultimate aim of designing nutritional approaches as an adjuvant therapeutic strategy.

Idiopathic pulmonary fibrosis (IPF) is characterized by an aberrant repair response with uncontrolled turnover of extracellular matrix involving mesenchymal cell phenotypes, where lung resident mesenchymal stem cells (LRMSC) have been supposed to have an important role. However, the contribution of LRMSC in lung fibrosis is not fully understood, and the role of LRMSC in IPF remains to be elucidated. Here, we performed transcriptomic and functional analyses on LRMSC isolated from IPF and control patients (CON). Both over-representation and gene set enrichment analyses indicated that oxidative phosphorylation is the major dysregulated pathway in IPF LRMSC. The most relevant differences in biological processes included complement activation, mesenchyme development, and aerobic electron transport chain. Compared to CON LRMSC, IPF cells displayed impaired mitochondrial respiration, lower expression of genes involved in mitochondrial dynamics, and dysmorphic mitochondria. These changes were linked to an impaired autophagic response and a lower mRNA expression of pro-apoptotic genes. In addition, IPF TGFβ-exposed LRMSC presented different expression profiles of mitochondrial-related genes compared to CON TGFβ-treated cells, suggesting that TGFβ reinforces mitochondrial dysfunction. In conclusion, these results suggest that mitochondrial dysfunction is a major event in LRMSC and that their occurrence might limit LRMSC function, thereby contributing to IPF development.

Lung-resident mesenchymal stem cells (LR-MSC) are thought to participate in idiopathic pulmonary fibrosis (IPF) by differentiating into myofibroblasts. On the other hand, LR-MSC in IPF patients present senescence-related features. It is unclear how they respond to a profibrotic environment. Here, we investigated the profibrotic response of LR-MSC isolated from IPF and control (CON) patients. LR-MSC were inoculated in mice 48 h after bleomycin (BLM) instillation to analyze their contribution to lung damage. In vitro, LR-MSC were exposed to TGFβ. Mice inoculated with IPF LR-MSC exhibited worse maintenance of their body weight. The instillation of either IPF or CON LR-MSC sustained BLM-induced histological lung damage, bronchoalveolar lavage fluid cell count, and the expression of the myofibroblast marker, extracellular matrix (ECM) proteins, and proinflammatory cytokines in the lungs. In vitro, IPF LR-MSC displayed higher basal protein levels of aSMA and fibronectin than CON LR-MSC. However, the TGFβ response in the expression of TGFβ, aSMA, and ECM genes was attenuated in IPF LR-MSC. In conclusion, IPF LR-MSC have acquired myofibroblastic features, but their capacity to further respond to profibrotic stimuli seems to be attenuated. In an advanced stage of the disease, LR-MSC may participate in disease progression owing to their limited ability to repair epithelial damage.

Monitoring and control of indoor air hygiene has gained much interest since the COVID-19 pandemic because the airborne route is the main pathway for the spread of SARS-CoV-2 and other pathogens, making it necessary to develop strategies to mitigate airborne transmission of diseases. This work addresses indoor breathable air hygiene by proposing the “in situ” reduction of airborne microorganisms with the nebulization of low and safe concentrations of hydrogen peroxide (H₂O_2, 0.5 and 1 ppm), ozone (O_3, 0.06 and 0.2 ppm), triethylene glycol (TEG, 17.1, 52 and 171.2 ppm), and their combinations. The antimicrobial activity was evaluated in an office room by assessing the viability of commercial extremophile sporulated bacteria and naturally present bacteria and fungi in surfaces and air. All three chemicals individually dispersed reduced the viability of sporulated bacteria and naturally occurring microorganisms. Binary combinations were more effective than individual agents in the case of the H₂O₂ and O₃ mixture against sporulated bacteria, and the O₃ and TEG mixture against airborne and surface bacteria. The ternary mixture was the most effective against commercial sporulated bacteria and airborne microorganisms. These results illustrate that the application of low and safe concentrations of antimicrobial compounds in indoor air could be an interesting strategy to reduce infection risk.

There is a paucity of in vivo assays to investigate the potential deleterious effects of plastic-laden compounds in the gastrointestinal tract of mammals, compared to in vitro testing and ecotoxicity assays in marine organisms. This work aims to fill this gap through a comprehensive evaluation of the acute toxicokinetics and bioavailability of bisphenol A (BPA)-adsorbed medium-density polyethylene (PE) microplastics (MPs) (ca. 3000 μg BPA/g), with a mean particle size of 136 μm, which were administered via oral gavage at a mere 0.67 mg BPA/kg body weight for 24 h using a murine model. The determination of plasma BPA-glucuronide revealed that BPA associated with MPs (PE-BPA) is bioavailable to a similar extent to that of freely dissolved BPA, with Area Under the Curves (AUC) values of 1249 ± 182 and 928 ± 276 μg h·L^-1 for the 0 → 6 h interval (AUC_0→6h), and 3586 ± 526 and 2325 ± 634 μg h·L^-1 for the 0 → 24 h interval (AUC_0→24h), corresponding to PE-BPA and free BPA, respectively. Several biomarker assays of the small intestine and liver, and the investigation of the gut barrier function were conducted to elucidate the potential deleterious effects of PE-BPA as compared to BPA and PE alone. Acute exposure to PE-BPA increased the expression of the detoxification biomarkers multidrug resistance protein 1 (MDR1) and UDP-glucuronosyltransferase 2b1 (UGT2b1) in the jejunum, particularly when PE and BPA occurred together, likely due to the extended intestinal residence time of the BPA-laden MPs. Oxidative stress markers, such as superoxide dismutase activity, and inflammatory responses, evaluated by myeloperoxidase activity, were also elevated in the PE-BPA group, suggesting a defensive response but without evidence of oxidative damage as determined by the malondialdehyde levels. In conclusion, the findings suggest that BPA associated with MPs exhibits similar bioavailability than that of freely dissolved BPA, with the subsequent activation of detoxification pathways and inflammatory responses.

Understanding the COVID-19 patient characteristics that impact environmental SARS-CoV-2 load is essential for improving infection risk management. In this study, we analyzed the influence of patient variables on airborne SARS-CoV-2 genome detection. Sixty-nine COVID-19 patients were recruited across three independent studies with airborne SARS-CoV-2 genome assessed in individual hospital rooms using droplet digital PCR. In the bivariate analysis, the odds of airborne SARS-CoV-2 detection were significantly higher for patients with obesity, chronic respiratory diseases, pneumonia at admission, sampling, and discharge, and lower lymphocytes count. No significant associations were found between airborne SARS-CoV-2 detection and symptoms presence or duration, nor with the results of the most recent positive nasopharyngeal PCR test prior to air sampling. In the multivariate analysis, the best-fit model included patient age, type of admission, and symptoms duration. Patient age significantly contributed to the risk of airborne SARS-CoV-2 detection in the multivariate analysis. Our findings highlight the variability in individual responses to SARS-CoV-2 infection and suggest that factors linked to COVID-19 severity, symptomatology, and immunocompetence influence the airborne SARS-CoV-2 detection. Our results may support the development of more precise preventive measures in healthcare settings.