Induction of Heat Stress Proteins Is Associated with Decreased Mortality in an Animal Model of Acute Lung Injury

1993 ◽  
Vol 147 (1) ◽  
pp. 177-181 ◽  
Author(s):  
Jesus Villar ◽  
Jeffrey D. Edelson ◽  
Martin Post ◽  
J. Brendan M. Mullen ◽  
Arthur S. Slutsky
Keyword(s):  
Animal Model ◽  
Heat Stress ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Stress Proteins ◽  
Heat Stress Proteins

Association Between Heat Stress Protein 70 Induction and Decreased Pulmonary Fibrosis in an Animal Model of Acute Lung Injury

Lung ◽  
2007 ◽  
Vol 185 (5) ◽  
pp. 287-293 ◽  
Author(s):  
Satoshi Hagiwara ◽  
Hideo Iwasaka ◽  
Shigekiyo Matsumoto ◽  
Takayuki Noguchi ◽  
Hidekatsu Yoshioka
Keyword(s):  
Animal Model ◽  
Heat Stress ◽  
Acute Lung Injury ◽  
Pulmonary Fibrosis ◽  
Lung Injury ◽  
Stress Protein ◽  
Heat Stress Protein

scholarly journals Rat model of smoke inhalation-induced acute lung injury

2021 ◽  
Vol 8 (1) ◽  
pp. e000879
Author(s):  
Premila Devi Leiphrakpam ◽  
Hannah R Weber ◽  
Tobi Ogun ◽  
Keely L Buesing
Keyword(s):  
Animal Model ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Caspase 3 ◽  
Small Animal ◽  
Therapeutic Options ◽  
Smoke Inhalation ◽  
Small Animal Model ◽  
Injury Score ◽  
Confounding Variables

BackgroundAcute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a lethal disease with limited therapeutic options and an unacceptably high mortality rate. Understanding the complex pathophysiological processes involved in the development of ALI/ARDS is critical for developing novel therapeutic strategies. Smoke inhalation (SI) injury is the leading cause of morbidity and mortality in patients with burn-associated ALI/ARDS; however, to our knowledge few reliable, reproducible models are available for pure SI animal model to investigate therapeutic options for ALI/ARDS without the confounding variables introduced by cutaneous burn or other pathology.ObjectiveTo develop a small animal model of pure SI-induced ALI and to use this model for eventual testing of novel therapeutics for ALI.MethodsRats were exposed to smoke using a custom-made smoke generator. Peripheral oxygen saturation (SpO2), heart rate, arterial blood gas, and chest X-ray (CXR) were measured before and after SI. Wet/dry weight (W/D) ratio, lung injury score and immunohistochemical staining of cleaved caspase 3 were performed on harvested lung tissues of healthy and SI animals.ResultsThe current study demonstrates the induction of ALI in rats after SI as reflected by a significant, sustained decrease in SpO2 and the development of diffuse bilateral pulmonary infiltrates on CXR. Lung tissue of animals exposed to SI showed increased inflammation, oedema and apoptosis as reflected by the increase in W/D ratio, injury score and cleaved caspase 3 level of the harvested tissues compared with healthy animals.ConclusionWe have successfully developed a small animal model of pure SI-induced ALI. This model is offered to the scientific community as a reliable model of isolated pulmonary SI-induced injury without the confounding variables of cutaneous injury or other systemic pathology to be used for study of novel therapeutics or other investigation.

scholarly journals The Heat Stress Transcription Factor LlHsfA4 Enhanced Basic Thermotolerance through Regulating ROS Metabolism in Lilies (Lilium Longiflorum)

2022 ◽  
Vol 23 (1) ◽  
pp. 572
Author(s):  
Chengpeng Wang ◽  
Yunzhuan Zhou ◽  
Xi Yang ◽  
Bing Zhang ◽  
Fuxiang Xu ◽  
...  
Keyword(s):  
Heat Stress ◽  
Stress Response ◽  
Stress Proteins ◽  
Lilium Longiflorum ◽  
Ros Scavenging ◽  
Heat Stress Response ◽  
Ros Metabolism ◽  
Heat Stress Proteins ◽  
Dependent Pathway ◽  
Heat Stress Transcription Factors

Heat stress severely affects the annual agricultural production. Heat stress transcription factors (HSFs) represent a critical regulatory juncture in the heat stress response (HSR) of plants. The HsfA1-dependent pathway has been explored well, but the regulatory mechanism of the HsfA1-independent pathway is still under-investigated. In the present research, HsfA4, an important gene of the HsfA1-independent pathway, was isolated from lilies (Lilium longiflorum) using the RACE method, which encodes 435 amino acids. LlHsfA4 contains a typical domain of HSFs and belongs to the HSF A4 family, according to homology comparisons and phylogenetic analysis. LlHsfA4 was mainly expressed in leaves and was induced by heat stress and H2O2 using qRT-PCR and GUS staining in transgenic Arabidopsis. LlHsfA4 had transactivation activity and was located in the nucleus and cytoplasm through a yeast one hybrid system and through transient expression in lily protoplasts. Over expressing LlHsfA4 in Arabidopsis enhanced its basic thermotolerance, but acquired thermotolerance was not achieved. Further research found that heat stress could increase H2O2 content in lily leaves and reduced H2O2 accumulation in transgenic plants, which was consistent with the up-regulation of HSR downstream genes such as Heat stress proteins (HSPs), Galactinol synthase1 (GolS1), WRKY DNA binding protein 30 (WRKY30), Zinc finger of Arabidopsis thaliana 6 (ZAT6) and the ROS-scavenging enzyme Ascorbate peroxidase 2 (APX2). In conclusion, these results indicate that LlHsfA4 plays important roles in heat stress response through regulating the ROS metabolism in lilies.

scholarly journals The effects of Gamijinhae-tang on elastase/lipopolysaccharide-induced lung inflammation in an animal model of acute lung injury

2013 ◽  
Vol 13 (1) ◽  
Author(s):  
Sung-Hwa Sohn ◽  
HaRyeon Jang ◽  
Youngeun Kim ◽  
Young Pyo Jang ◽  
Seung-Hun Cho ◽  
...  
Keyword(s):  
Animal Model ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Lung Inflammation

Effects of Vaporized Perfluorocarbon on Surfactant Proteins in an Animal Model of LPS-Induced Acute Lung Injury

CHEST Journal ◽  
2016 ◽  
Vol 149 (4) ◽  
pp. A154
Author(s):  
BingChao Han ◽  
Kun Xiao ◽  
LongXiang Su ◽  
Youning Liu ◽  
Lixin Xie
Keyword(s):  
Animal Model ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Surfactant Proteins

Heat-Stress Proteins and Thermal Resistance in Rat Mammary Tumor Cells

1983 ◽  
Vol 95 (2) ◽  
pp. 399 ◽  
Author(s):  
Stephen P. Tomasovic ◽  
Peter A. Steck ◽  
Daragh Heitzman
Keyword(s):  
Heat Stress ◽  
Thermal Resistance ◽  
Tumor Cells ◽  
Mammary Tumor ◽  
Stress Proteins ◽  
Mammary Tumor Cells ◽  
Rat Mammary Tumor ◽  
Heat Stress Proteins

UVB Light Exposed Human Platelets Mediate Acute Lung Injury In a Two-Event Mouse Model of Transfusion

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 3354-3354
Author(s):  
Monique Gelderman-Fuhrmann ◽  
Xuan Chi ◽  
Li Zhi ◽  
Jaroslav Vostal
Keyword(s):  
Animal Model ◽  
Acute Lung Injury ◽  
Confocal Microscopy ◽  
Lung Injury ◽  
Conflicts Of Interest ◽  
Species Difference ◽  
Human Platelets ◽  
Lung Damage ◽  
Organ Distribution ◽  
Leukocyte Accumulation

Abstract Abstract 3354 Transfusion related acute lung injury (TRALI) has occurred in patients whose underlying condition led to an inflamed endothelium, and who were transfused with a transfusion product that contained either HLA or HNA antibodies or biologic modifiers such as lipids or antigens from stored cells. Similar two-event reactions can be modeled in animals pretreated with lipopolysaccharide (LPS) and infused with similar types of antibodies or media from stored transfusion products. The first event induces activation of the endothelium and sequestration of neutrophils in the lungs while the second event activates neutrophils to cause local tissue damage. In some animal models of acute lung damage platelet depletion reduces the lung damage while in other models infusion of activated platelets potentiates it. Ultraviolet B (UVB) light has been used on platelet transfusion products to prevent alloimmunization or with chemical sensitizers to reduce pathogens. Such processing may damage platelets and potentiate their storage lesion. UVB exposed human platelets (HPs) were evaluated in a two-event animal model of acute lung injury (ALI) where the sensitizing event was LPS and the second event was infusion of HPs or UVB HPs (2.4 J/cm2). Immunodeficient (SCID) mice were used to minimize the species difference (Piper et al., Transfusion 47:1540-9, 2007). UVB exposure of HPs increased their p-selectin expression (control 17.8±0.3% vs. UVB 35.9±3.2%) and reduced their JC-1 dye ratio indicating mitochondrial damage (8.9±0.7 control vs 1.9±1.2 UVB). Internal organ distribution of intravenous (IV) infused HPs was followed with whole animal imaging, confocal microscopy and with pathophysiological changes in bronchoalveolar lavage fluid (BALF). In LPS-treated mice, UVB HPs labeled with fluorescent dye had more accumulation in lungs compared to untreated HPs (29±12% vs 15±5% respectively; % of total fluorescence recovered), while the accumulation in lungs of healthy animals was equivalent for both UVB treated and untreated HPs. In separate experiments, LPS pretreated mice were infused with UVB exposed HPs or control HPs, and lungs were examined by histology and with confocal microscopy for fluorescent staining for CD41 and CD62 expression. Histology sections revealed extensive changes in lungs, such as thickening of the alveolar septa and obliteration of lung architecture in LPS animals infused with UVB HPs as compared to healthy animals infused with control HPs or with HPs treated with UVB. Confocal microscopy with specific antibodies identified HP accumulation in lungs of LPS treated animals infused with UVB exposed HPs. However, HP accumulation in lungs did not occur with control HPs or in healthy mice. Accumulation of UVB HPs in lungs of LPS pretreated mice was associated with increased (3-4 fold compared to control HPs) protein concentration and leukocyte accumulation in BALF. Increased alveolar permeability to protein and leukocyte accumulation in alveoli is associated with acute lung damage. To examine whether lung damage occurred due to presence of UVB HPs in the lungs or due to biologic mediators released into plasma from UVB exposed HPs we separated plasma from HPs post UVB treatment and infused the UVB plasma alone. Plasma isolated from UVB HPs did not alter BALF protein levels or leukocyte counts even though the UVB HPs did. In conclusion, UVB HPs can accumulate in lungs of LPS primed animals and are associated with lung damage as indicated by histological changes and increased protein and WBCs in BALF fluid. The ALI is associated with direct platelet accumulation in the lungs but not with biologic modifiers released into plasma. Our animal model of ALI suggests that HPs exposed to high doses of UVB could mediate similar effects in patients predisposed to TRALI with sepsis or other causes of endothelial cell inflammation. The findings and conclusions in this abstract have not been formally disseminated by the Food and Drug Administration and should not be construed to represent any Agency determination or policy. Disclosures: No relevant conflicts of interest to declare.

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