Microplastic biofilms, known as the “plastisphere”, harbor diverse microbial communities and serve as reservoirs for antibiotic resistance genes (ARGs). This review discussed the mechanisms driving bacterial community alteration on microplastics and delineated the pathways through which ARGs transfer within microplastic biofilms. We expected to provide a comprehensive understanding of the ecological and human health impacts associated with microplastic biofilms and ARGs, thereby informing strategies to mitigate plastic pollution and its risks.

Mounting data suggest that environmental pollution due to airborne fine particles (AFPs) increases the occurrence and severity of respiratory virus infection in humans. However, it is unclear whether and how interactions with AFPs alter viral infection and distribution. We report synergetic effects between various AFPs and the H1N1 virus, regulated by physicochemical properties of the AFPs. Unlike infection caused by virus alone, AFPs facilitated the internalization of virus through a receptor-independent pathway. Moreover, AFPs promoted the budding and dispersal of progeny virions, likely mediated by lipid rafts in the host plasma membrane. Infected animal models demonstrated that AFPs favored penetration of the H1N1 virus into the distal lung, and its translocation into extrapulmonary organs including the liver, spleen, and kidney, thus causing severe local and systemic disorders. Our findings revealed a key role of AFPs in driving viral infection throughout the respiratory tract and beyond. These insights entail stronger air quality management and air pollution reduction policies.

Exposure routes and transport of microplastics (MPs) from the environment into the human bodies deserve considerable attention. Intravenous injection has been reported as a direct MP-intrusion pathway. However, it is unclear whether or how the infusion fluid composition influences polymer degradation and MP release. Here, we determined that the concentrations of MPs shed from infusion bags ranged from 522 to 5455 particles/L. The storage period, mechanical shaking, and storage temperature all contributed to MP release to some extent; however, the infusion fluid composition affected the formation of MPs more than any other factor. Infusion fluids containing moxifloxacin hydrochloride, etimicin sulfate, and sodium bicarbonate ringer's solution generated more reactive oxygen species than those containing sodium chloride, grape sugar, and glucose and sodium chloride. Specifically, the generation of reactive oxygen species (hydroxyl radicals, carbonate radicals, and single oxygen) facilitated oxygen-containing functional group formation and breaking of carbon chains on the surface of the polypropylene plastic, which increased aging and fragmentation. Overall, this study provides knowledge of the mechanisms underlying MP release from infusion bags during storage and transportation. This offers insight for optimizing the use and handling of infusion bags in medical settings to minimize contamination.

Pneumoconiosis is a progressive and life-threatening fibrotic lung disorder caused by the prolonged deposition of inhaled particulate matters (PMs); thus far, no cure is available. Emerging evidence has suggested that the resulting disordered respiratory microbiome is caused by disturbed lung architecture and homeostasis responding to inhalable PMs. Lung microbiome dysbiosis also contributes to injury to the lung and distant organs, such as the intestine, through the lung-gut axis. Current studies on the microbiome-disease interplay are still in their infancy, and sufficient understanding of microbial heterogeneity in pathological processes is lacking. Here we investigated the microbiome in the lung and gut of patients with pneumoconiosis in comparison to healthy individuals. Our findings indicated reciprocal causation between lung injuries and microbial dysbiosis under particle exposure; pulmonary Streptococcus and Stenotrophomonas, along with intestinal Ligilactobacillus and Blautia, may represent key microbial communities influencing pneumoconiosis progression. We defined close microbiota crosstalk between the lung and gut, as evidenced by their interaction networks, implying considerable effects on the gut microenvironment through either direct microbial translocation or other mechanisms such as inflammation-driven alterations. Animal experiments further corroborated the findings in humans. Collectively, our results highlight the potential involvement of the lung-gut axis microbial dysbiosis in pneumoconiosis pathogenesis and open a new avenue to develop microbiome-targeted diagnosis and treatment strategies.

The heterogeneity of pulmonary cells affects their response to inhaled fine particles. However, the most critical responder cells in particle exposure still remain controversial, and their functional heterogeneity warrants detailed exploration. Herein, a gold nanoparticle model dual‐labeled with sulfo‐cyanine3 and Tag RNAs is developed, aiming to capture prominent fine particle–responsive cell subpopulations using fluorescence‐activated cell sorting and single‐cell RNA sequencing. Alveolar macrophages (AMs), recruited macrophages (recMacs), and interstitial macrophages (IMs) exhibited the strongest responsiveness to particles, among which 14 subsets are identified with partially overlapping yet distinct functions. Notably, AMs_3, AMs_7, and recMacs_4 subsets are highlighted in the particle–responsive single‐cell atlas, as evinced from their functional scoring and Tag RNA levels. AMs_3 and AMs_7 showed function enrichment for acute‐phase responses to inhaled particles, while recMacs_4 exhibited enrichment for cell chemotaxis and phagocytosis. Fine particle engulfment led to enhanced outgoing interactions between these three macrophage subsets and other cell populations within particle–responsive cellular communication networks. This study reveals that specific macrophage subpopulations act as the primary responsive cell subpopulations in engulfing inhaled particles and link their transcriptional heterogeneity to functional diversity, thereby opening a new avenue to explore the heterogeneity of immune cells in pulmonary disorders.

• The microbiota of healthy lungs changes over time and forms a dynamic balance. • Microbiome dysbiosis links to various respiratory diseases, including asthma and IPF. • The lung microbiota regulates pulmonary diseases by modulating immune cell function.