scholarly journals A Case of Acute Lung Failure: Administration of Exogenous Surfactant As A Successful Treatment

2020 ◽  
Vol 5 (1) ◽  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Haemorrhagic Shock ◽  
Exogenous Surfactant ◽  
Repeated Treatment ◽  
Rapid Improvement ◽  
Acute Lung Failure ◽  
Fractional Dose ◽  
Lung Failure

We are describing a case of acute lung injury associated with uraemia and haemorrhagic shock. The treatment has consisted of the administration of repeated and equal doses of exogenous surfactant for 72 hours, starting within 48 hours from the beginning of the symptoms. A rapid improvement in the lung function has been detected, with consequent weaning from mechanical ventilation. The CT scan has confirmed the enhancement of atelectasis and hypoventilation. This case highlights the pivotal role of the administration of exogenous surfactant in selected cases of acute lung injury. If an anti-inflammatory effect is needed, we suppose that a repeated treatment with fractional dose is more effective.

Role of exogenous surfactant in acute lung injury

2003 ◽  
Vol 31 (Supplement) ◽  
pp. S324-S328 ◽  
Author(s):  
James F. Lewis ◽  
Angela Brackenbury
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Exogenous Surfactant

scholarly journals RAGE-induced ILC2 expansion in acute lung injury due to haemorrhagic shock

Thorax ◽  
2020 ◽  
Vol 75 (3) ◽  
pp. 209-219 ◽  
Author(s):  
Kai Zhang ◽  
Yue Jin ◽  
Dengming Lai ◽  
Jieyan Wang ◽  
Yang Wang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Immune Responses ◽  
Immune Dysfunction ◽  
Underlying Mechanism ◽  
Haemorrhagic Shock ◽  
Lymphoid Cells ◽  
Eosinophil Infiltration

BackgroundType 2 immune dysfunction contributes to acute lung injury and lethality following haemorrhagic shock (HS) and trauma. Group 2 innate lymphoid cells (ILC2s) play a significant role in the regulation of type 2 immune responses. However, the role of ILC2 in post-HS acute lung injury and the underlying mechanism has not yet been elucidated.ObjectiveTo investigate the regulatory role of ILC2s in HS-induced acute lung injury and the underlying mechanism in patients and animal model.MethodsCirculating markers of type 2 immune responses in patients with HS and healthy controls were characterised. Using a murine model of HS, the role of high-mobility group box 1 (HMGB1)-receptor for advanced glycation end products (RAGE) signalling in regulation of ILC2 proliferation, survival and function was determined. And the role of ILC2 in inducing type 2 immune dysfunction was assessed as well.ResultsThe number of ILC2s was significantly increased in the circulation of patients with HS that was correlated with the increase in the markers of type 2 immune responses in the patients. Animal studies showed that HMGB1 acted via RAGE to induce ILC2 accumulation in the lungs by promoting ILC2 proliferation and decreasing ILC2 death. The expansion of ILC2s resulted in type 2 cytokines secretion and eosinophil infiltration in the lungs, both of which contributed to lung injury after HS.ConclusionsThese results indicate that HMGB1-RAGE signalling plays a critical role in regulating ILC2 biological function that aggravates type 2 lung inflammation following HS.

Corrigendum to ‘Platonin mitigates acute lung injury in haemorrhagic shock rats’ [Resuscitation 82 (2011) 97–104]

Resuscitation ◽  
2013 ◽  
Vol 84 (3) ◽  
pp. 397-398
Author(s):  
Hsi-Ning Chu ◽  
Pei-Shan Tsai ◽  
Tao-Yeuan Wang ◽  
Chun-Jen Huang
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Haemorrhagic Shock

scholarly journals Leukocyte immunoglobulin-like receptor B4 deficiency exacerbates acute lung injury via NF-κB signaling in bone marrow-derived macrophages

2019 ◽  
Vol 39 (6) ◽  
Author(s):  
Tao Qiu ◽  
Jiangqiao Zhou ◽  
Tianyu Wang ◽  
Zhongbao Chen ◽  
Xiaoxiong Ma ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Stromal Cells ◽  
Marrow Cell ◽  
Marrow Transplant ◽  
Cell Source ◽  
Transplant Model ◽  
Acute Inflammatory Disease

AbstractAcute lung injury (ALI) is an acute inflammatory disease. Leukocyte immunoglobulin-like receptor B4 (LILRB4) is an immunoreceptor tyrosine-based inhibitory motif (ITIM)-bearing inhibitory receptor that is implicated in various pathological processes. However, the function of LILRB4 in ALI remains largely unknown. The aim of the present study was to explore the role of LILRB4 in ALI. LILRB4 knockout mice (LILRB4 KO) were used to construct a model of ALI. Bone marrow cell transplantation was used to identify the cell source of the LILRB4 deficiency-aggravated inflammatory response in ALI. The effect on ALI was analyzed by pathological and molecular analyses. Our results indicated that LILRB4 KO exacerbated ALI triggered by LPS. Additionally, LILRB4 deficiency can enhance lung inflammation. According to the results of our bone marrow transplant model, LILRB4 regulates the occurrence and development of ALI by bone marrow-derived macrophages (BMDMs) rather than by stromal cells in the lung. The observed inflammation was mainly due to BMDM-induced NF-κB signaling. In conclusion, our study demonstrates that LILRB4 deficiency plays a detrimental role in ALI-associated BMDM activation by prompting the NF-κB signal pathway.

H2O2 inhibits alveolar epithelial wound repair in vitro by induction of apoptosis

2004 ◽  
Vol 287 (2) ◽  
pp. L448-L453 ◽  
Author(s):  
Thomas Geiser ◽  
Masanobu Ishigaki ◽  
Coretta van Leer ◽  
Michael A. Matthay ◽  
V. Courtney Broaddus
Keyword(s):  
Acute Lung Injury ◽  
Epithelial Cells ◽  
Lung Injury ◽  
Cell Viability ◽  
Wound Repair ◽  
Wound Edge ◽  
Alveolar Epithelial ◽  
Induction Of Apoptosis

Reactive oxygen species (ROS) are released into the alveolar space and contribute to alveolar epithelial damage in patients with acute lung injury. However, the role of ROS in alveolar repair is not known. We studied the effect of ROS in our in vitro wound healing model using either human A549 alveolar epithelial cells or primary distal lung epithelial cells. We found that H2O2 inhibited alveolar epithelial repair in a concentration-dependent manner. At similar concentrations, H2O2 also induced apoptosis, an effect seen particularly at the edge of the wound, leading us to hypothesize that apoptosis contributes to H2O2-induced inhibition of wound repair. To learn the role of apoptosis, we blocked caspases with the pan-caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp (zVAD). In the presence of H2O2, zVAD inhibited apoptosis, particularly at the wound edge and, most importantly, maintained alveolar epithelial wound repair. In H2O2-exposed cells, zVAD also maintained cell viability as judged by improved cell spreading and/or migration at the wound edge and by a more normal mitochondrial potential difference compared with cells not treated with zVAD. In conclusion, H2O2 inhibits alveolar epithelial wound repair in large part by induction of apoptosis. Inhibition of apoptosis can maintain wound repair and cell viability in the face of ROS. Inhibiting apoptosis may be a promising new approach to improve repair of the alveolar epithelium in patients with acute lung injury.

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