Remote Ischemic Conditioning Reduced Acute Lung Injury After Traumatic Brain Injury in the Mouse

Abstract

Traumatic brain injury (TBI) can induce acute lung injury (ALI). The exact pathomechanism of TBI-induced ALI is poorly understood, limiting treatment options. Remote ischemic conditioning (RIC) can mitigate detrimental outcomes following transplants, cardiac arrests, and neurological injuries. In this study, we hypothesized that RIC would reduce TBI-induced ALI by regulating the sphingosine-1-phosphate (S1P)-dependent pathway, a central regulator of endothelial barrier integrity, lymphocyte, and myokine trafficking. Male mice were subjected to either diffuse TBI by midline fluid percussion or control sham injury and randomly assigned among four groups: sham, TBI, sham RIC, or TBI RIC; RIC was performed 1 h prior to TBI. Mice were euthanized at 1-h postinjury or 7 days post-injury (DPI) and lung tissue, bronchoalveolar lavage (BAL) fluid, and blood were collected. Lung tissue was analyzed for histopathology, irisin myokine levels, and S1P receptor levels. BAL fluid and blood were analyzed for cellularity and myokine/S1P levels, respectively. One-hour postinjury, TBI damaged lung alveoli and increased neutrophil infiltration; RIC preserved alveoli. BAL from TBI mice had more neutrophils and higher neutrophil/monocyte ratios compared with sham, where TBI RIC mice showed no injury-induced change. Further, S1P receptor 3 and irisin-associated protein levels were significantly increased in the lungs of TBI mice compared with sham, which was prevented by RIC. However, there was no RIC-associated change in plasma irisin or S1P. At 7 DPI, ALI in TBI mice was largely resolved, with evidence for residual lung pathology. Thus, RIC may be a viable intervention for TBI-induced ALI to preserve lung function and facilitate clinical management.

Experimental diffuse brain injury and a model of Alzheimer's disease exhibit disease‐specific changes in sleep and incongruous peripheral inflammation

“…Surgeries/injuries were performed on 16 WT Aged mice. Two WT Aged mice died from brain injury‐induced pulmonary edema <30 min after injury (Saber et al., 2020). Therefore, a total of 30 mice were used for data analyses: 16 3xTg‐AD mice and 14 WT Aged TBI mice.…”

“…Surgeries/injuries were performed on 16 WT Aged mice. Two WT Aged mice died from brain injuryinduced pulmonary edema <30 min after injury (Saber et al, 2020).…”

Mir-204 Regulates LPS-Induced A549 Cell Damage by Targeting FOXK2

“…Hirsutanol A (HA) has a strong cytotoxic effect as a sessile mushroom compound. Studies have found that HA can induce tumor cell apoptosis by upregulating cleaved-caspase-3, but it is rarely reported in ALI and ARDS [ 6 , 7 ].…”

Irisin Activates M1 Macrophage and Suppresses Th2-Type Immune Response in Rats with Pelvic Inflammatory Disease

“…Studies have shown that, during acute lung injury, irisin protects alveolar epithelial cells from damage by maintaining mitochondrial function and improving oxidative stress [ 19 ]. In addition, in the research of brain injury and type 2 diabetes, the effects on antioxidative stress, antiapoptosis, and anti-inflammatory are also described [ 20 , 21 ]. In this study, we first detected serum cytokine levels and found that irisin dramatically reduced the level of inflammation in rats with APID.…”