Pathological damage, immune-related protein expression, and oxidative stress in lungs of BALB/c mice induced by haze PM2.5 biological components exposure

Abstract

Particulate matter (PM) pollution poses a huge public health threat, and exposure to haze pollution for short or long periods of time cause health problems. In this study, 16S rDNA and ITS high-throughput sequencing were used to analyze the microbial components of fine particulate matter (PM2.5) collected between December 20th and December 27th of 2016 during a severe haze in Tai'an, China. Although most inhalable microorganisms are not pathogenic to humans, we detected the presence of some types of bacteria that cause respiratory inflammation (such as Pseudomonas and Corynebacterium), allergic reactions (such as Alternaria), and lung inflammation (such as Nesterenkonia). Acute and chronic haze PM2.5 exposure experiments were conducted using BALB/c mice to gain insight about the harm these microbes may have on human health. Results indicate that acute exposure to haze PM2.5 can cause pathological lung damage, decrease the expressions of oxidative stress indicators T-AOC, SOD, and GSH-PX, increase the expression of MDA, and induce apoptosis. Furthermore, chronic exposure was found to cause more damage. Toll-like receptors can be used identify molecular patterns associated with microbial pathogens. The expression of TLR2 and TLR4 were increased in both single- and repeated-exposure groups, but they were significantly increased in the repeated-exposure group (P < 0.05). The role of biological components in PM in mediating inflammation and pathological damage should not be neglected.