Abstract

Exposure to particulate matter (PM) is associated with increased incidence of respiratory diseases. The present study aimed to investigate the roles of fibroblast growth factor 10 (FGF10) in PM-induced lung injury. Mice were intratracheally instilled with FGF10 or phosphate-buffered saline at one hour before instillation of PM for two consecutive days. In addition, the anti-inflammatory impact of FGF10 in vitro and its effect on the high-mobility group box 1 (HMGB1)-toll-like receptor 4 (TLR4) pathway was investigated. It was found that PM exposure is associated with increased inflammatory cell infiltration into the lung and increased vascular protein leakage, while FGF10 pretreatment attenuated both of these effects. FGF10 also decreased the PM-induced expression of interleukin (IL)-6, IL-8, tumor necrosis factor-α and HMGB1 in murine bronchoalveolar lavage fluid and in the supernatants of human bronchial epithelial cells exposed to PM. FGF10 exerted anti-inflammatory and cytoprotective effects by inhibiting the HMGB1-TLR4 pathway. These results indicate that FGF10 may have therapeutic values for PM-induced lung injury.

Highlights

  • Fine particulate matter (PM) is a prominent pollutant present in the air, and it represents a significant threat to public health, since a number of epidemiological studies have revealed that exposure to PM is associated with higher rates of asthma [1], chronic obstructive pulmonary disease [2], and lung cancer [3]

  • When the structural injury was assessed in the lung samples obtained from different treatment groups (n=3 mice/group), it was found that PM exposure was associated with a marked increase in acute lung inflammation, when compared to the lungs of control mice

  • PM exposure was associated with a significant increase in bronchoalveolar lavage fluid (BALF) protein levels, when compared to control mice, while fibroblast growth factor 10 (FGF10) pretreatment for one hour prior to PM exposure was associated to significantly reduced BALF protein levels in response to PM (Figure 1C)

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Summary

Introduction

Fine particulate matter (PM) is a prominent pollutant present in the air, and it represents a significant threat to public health, since a number of epidemiological studies have revealed that exposure to PM is associated with higher rates of asthma [1], chronic obstructive pulmonary disease [2], and lung cancer [3]. Due to the small size, these PM2.5 particles can readily be inhaled and deposited throughout the airways. The deposition of these particles in the alveoli can allow these to readily access capillaries and enter circulation, thereby leading to injury to a wide number of different tissues and organs [6,7]. Since it is difficult to control the environmental problems that drive the high PM level exposure, it is essential to identify alternative preventative or therapeutic approaches to protect the human respiratory system from PM-mediated respiratory injury

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