Lung macrophages are involved in lung injury secondary to repetitive diving

Abstract

This study aimed to establish an animal model of decompression-induced lung injury (DILI) secondary to repetitive diving in mice and explore the role of macrophages in DILI and the protective effects of high-concentration hydrogen (HCH) on DILI. Mice were divided into three groups: control group, DILI group, and HCH group. Mice were exposed to hyperbaric air at 600 kPa for 60 min once daily for consecutive 3 d and then experienced decompression. In HCH group, mice were administered with HCH (66.7% hydrogen and 33.3% oxygen) for 60 min after each hyperbaric exposure. Pulmonary function tests were done 6 h after decompression; the blood was harvested for cell counting; the lung tissues were harvested for the detection of inflammatory cytokines, hematoxylin and eosin (HE) staining, and immunohistochemistry; western blotting and polymerase chain reaction (PCR) were done for the detection of markers for M1 and M2 macrophages. Our results showed that bubbles formed after decompression and repeated hyperbaric exposures significantly reduced the total lung volume and functional residual volume. Moreover, repetitive diving dramatically increased proinflammatory factors and increased the markers of both M1 and M2 macrophages. HCH inhalation improved lung function to a certain extent, and significantly reduced the pro-inflammatory factors. These effects were related to the reduction of M1 macrophages as well as the increase in M2 macrophages. This study indicates that repetitive diving damages lung function and activates lung macrophages, resulting in lung inflammation. HCH inhalation after each diving may be a promising strategy for the prevention of DILI.

Hyperbaric Oxygen-Induced acute lung injury: A Mouse Model Study on Pathogenesis and Recovery Dynamics

“…ALI induced by hyperoxia may be due to direct damage from excess ROS production, or by exacerbating inflammation (24). Our findings indicate that HBO exposure significantly increases the expression levels of inflammatory and chemotactic cytokines, including Il6, Ccl2, Ccl3, and Cxcl10, consistent with previous research on normobaric hyperoxia-induced ALI (15)(16)(17)(18). However, under hyperbaric oxygen, significant increases in these factors are seen at 6 hours, whereas it takes at least 24 hours under normobaric conditions, with histological damage appearing at 48 hours (25).…”

“…Our previous has demonstrated increased expression of cytokines, cellular apoptosis and endothelial dysfunction, were significantly increased in lung injury induced by HBO exposure compared with room air controls, in rats (13) and mice (14). Excessive ROS leads to endothelial damage and inflammatory activation, resulting in increased expression of inflammatory cytokines and transcription factors in lung tissue (15), such as tumor necrosis factor (Tnf), interleukin 1 beta (Il1b), interleukin 6 (Il6), and interleukin 10 (Il10) (16)(17)(18). Additionally, ALI continues to progress even 24 hours after HBO exposure, and necroptosis may be involved in the pathology of ALI induced by hyperoxia (19).…”