Indoor dust exposure induces lung injury and disrupts the lung-bone marrow immune axis in C57BL/6J mice.

Since humans spend the majority of their time indoors, exposure to indoor dust is a primary route for air pollutant inhalation. Although growing evidence links indoor dust to respiratory impairments, the mechanisms underlying its association with lung damage and immune homeostasis remain poorly understood. In this study, indoor dust samples collected from an industrial city in Northern China (Taiyuan, Shanxi Province) were used to establish a mouse inhalation model at environmentally relevant concentrations. Non-invasive pulmonary function tests using the whole-body plethysmography (WBP) system and histopathological examinations revealed that indoor dust exposure induced significant impairments in lung function, characterized by a 33.34% increase in Penh and a 19.06% reduction in Rpef in the 25 mg/kg group, alongside airflow limitation (reduced ventilatory capacity) and airway obstruction (inflammatory narrowing of the respiratory tract). Exposure also caused alveolar structural damage, interstitial inflammatory infiltration, and pulmonary fibrosis. Transcriptomic profiling (RNA-seq), flow cytometric immunophenotyping, and qRT-PCR further demonstrated disruption of immune homeostasis in the bone marrow (BM). These results suggest a potential interorgan crosstalk between the lung and BM mediated by inflammatory signaling, in which the lung-derived inflammatory signals might alter the hematopoietic function of the BM, while the BM could mobilize immune cells to sustain pulmonary inflammatory responses, further contributing to lung function impairment. This interorgan crosslink offers a new clue for understanding the mechanisms underlying indoor dust-related lung injury through lung-BM immune communication and for identifying candidate intervention targets for environmental respiratory diseases.