Abstract
Fine particulate matter (PM(2.5)) has been widely regarded as an important environmental risk factor that has widely influenced health of both animals and humans. Lung injury is the main cause of PM(2.5) affecting respiratory tract health. Gut microbiota participates in the development of lung injury in many pathological processes. However, there is still unknown the specific effects of PM(2.5) on the gut-lung axis in broilers. Thus, we conducted a broiler model based on 3-wk-old male Arbor Acres broiler to explore the underlying mechanism. Our results showed that PM(2.5) exposure triggered TLR4 signaling pathway and induced the increase of IL-6, IFN-γ, TNF-α expression as well as the decrease of IL-10 expression in the lung. Inhaled PM(2.5) exposure significantly altered the gut microbiota diversity and community. Specifically, PM(2.5) exposure decreased α diversity and altered β diversity of gut microbiota, and reduced the abundance of DTU089, Oscillospirales, Staphylococcus, and increased the Escherichia-Shigella abundance, leading to the increase of gut-derived lipopolysaccharides (LPS). Moreover, PM(2.5) significantly disrupted the intestinal epithelial barrier by reducing the expression of muc2 and claudin-1 to increase intestinal permeability, which possibly facilitated the LPS translocation into the blood. Spearman analysis revealed that gut microbiota dysbiosis was positively related to TLR4, TNF-α, and IFN-γ expression in the lung. In summary, our results showed that PM(2.5) exposure induced lung injury by causing inflammation and triggering TLR4 signaling pathway, and also induced gut microbiota dysbiosis resulting in the overproduction of gut-derived LPS. And gut microbiota dysbiosis may be associated with lung injury. The above results provide basis data to comprehend the potential role of gut microbiota dysbiosis in the lung injury as well as providing a new regulatory target for alleviating lung injury associated with environmental pollutants.