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Acute Alveolar Injury: Experimental Models
Published in Joan Gil, Models of Lung Disease, 2020
The major links in the chain of events which leads to the protective action of neutrophils are now understood. When this sequence takes place locally, for example, at a site of tissue invasion by bacteria, the action is contained and the results tend to be beneficial or protective to the host. When it occurs massively and systemically in the vascular compartment, the results can be catastrophic. It has recently become apparent that damage can be inflicted upon the lung by just this chain of events which culminates with activated neutrophils sequestered in the pulmonary capillaries. While many questions remain unanswered, evidence is accumulating that the cascade of events culminating in this damage may play a major role in acute lung injury of diverse etiologies.
The Adult Respiratory Distress Syndrome and the Microcirculation
Published in John H. Barker, Gary L. Anderson, Michael D. Menger, Clinically Applied Microcirculation Research, 2019
Prognosis for recovery in ARDS depends on multiple factors. Patients who develop ARDS in association with sepsis have a significantly higher mortality than those who develop ARDS from aspiration of gastric contents, following major trauma, or from a primary pneumonia that is not associated with sepsis syndrome.2,10,11 There are several other factors that adversely affect the prognosis for survival including age over 60, the presence of nonpulmonary organ failure (such as renal failure, liver failure, hematologic failure, neurologic failure), metabolic acidosis at the onset of ARDS, and an underlying unfavorable medical diagnosis such as the presence of a hematologic malignancy or metastatic carcinoma.1–3, 10,12 As will be discussed in the section under treatment, therapeutic maneuvers for patients with ARDS must be directed both at treatment of the underlying cause of ARDS (such as sepsis) as well as providing supportive therapy for the respiratory failure and any other nonpulmonary organ failure, such as dialysis for renal failure. Prognosis may also be related to the severity of acute lung injury itself. For example, there is good evidence from our own clinical studies that some patients who develop ARDS have a more limited degree of acute lung injury with a greater capacity to resolve some of the pulmonary edema during the early phase of the syndrome. These patients may have less severe endothelial as well as less severe epithelial injury to the lung.13
Histopathology of interstitial lung disease: A pattern-based approach
Published in Muhunthan Thillai, David R Moller, Keith C Meyer, Clinical Handbook of Interstitial Lung Disease, 2017
Angela M Takano, Junya Fukuoka, Kevin O Leslie
This is the first histopathologic pattern to be considered because these instances are most often associated with an acute clinical presentation. Such conditions need immediate intervention (such as the case of diffuse alveolar haemorrhage with capillaritis) and can portend a high mortality rate (such as diffuse alveolar damage in cases of acute respiratory distress syndrome), or both (3). The pattern of acute lung injury is characterized by the presence of one or more of the following elements: interstitial oedema, intra-alveolar fibrinous exudates, reactive type 2 pneumocytes, hyaline membranes, tissue necrosis, intra-alveolar blood, haemosiderin-laden macrophages and intra-alveolar eosinophils.
Suberosin Alleviates Sepsis-Induced Lung Injury in A Rat Model of Cecal Ligation and Puncture
Published in Journal of Investigative Surgery, 2023
Sevgi Karabulut Uzunçakmak, Zekai Halıcı, Songül Karakaya, Zerrin Kutlu, Yavuz Selim Sağlam, İsmail Bolat, Pelin Aydın, Ceyda Sibel Kılıç
Acute lung injury and ARDS are observed frequently in cases of sepsis [3,24]. The lung pathology seen in sepsis entails the damage of alveolar epithelial cells and alveolar capillary endothelial cells, together with alveolar edema and pulmonary accumulation of neutrophils [35]. When an unusual microbial presence is detected, endothelial cells produce proinflammatory cytokines and chemokines that increase the immune response [36]. In our sepsis model (CLP group), increased interalveolar septal thickening, desquamation of the bronchial epithelium, and venous hyperemia were observed. SBR attenuated these alterations in a dose-dependent manner in the SBR1, SBR2, and SBR3 groups. Lung tissues in the SBR group were similar to the control group. These results suggest that SBR may be capable of ameliorating sepsis-related lung damage.
Melatonin attenuates lung ischemia-reperfusion injury through SIRT3 signaling-dependent mitophagy in type 2 diabetic rats
Published in Experimental Lung Research, 2023
Zhiqiang Song, Congmin Yan, Yuanbo Zhan, Qiujun Wang, Yina Zhang, Tao Jiang
Acute lung injury is commonly encountered in hospital and outpatient settings and remains a leading cause of patient morbidity and mortality. Many medical conditions, such as pulmonary embolism, acute respiratory distress syndrome (ARDS), cardiopulmonary bypass surgery, and lung transplantation can cause ischemia reperfusion–induced lung injuries.1 The global prevalence of diabetes mellitus (DM) is significantly increasing across all age groups.2 Emerging data suggest the lung is a target of diabetic injury, and DM is a significant risk factor for mortality at both 1 and 5 years after lung transplantation.3 Previously, we reported that DM exacerbated lung ischemia-reperfusion injury (LIRI) in type 2 diabetic rats, and mitochondrial dysfunction play a central role in diabetic LIRI.4,5 To this end, preservation of mitochondrial function under type 2 DM represents a potential therapeutic target for treatment of LIRI.
Da-Yuan-Yin decoction polyphenol fraction attenuates acute lung injury induced by lipopolysaccharide
Published in Pharmaceutical Biology, 2023
Lengqiu Guo, Yun Yang, Jie Yuan, Huiling Ren, Xiaolei Huang, Meng Li, Long Xia, Xiaogang Jiang, Daofeng Chen, Jian Zhang
Acute lung injury (ALI) originates from many direct and indirect injury factors. Its severe form is acute respiratory distress syndrome (ARDS). The main pathological features of ALI are diffuse lung cell injury, inflammatory cell infiltration in lung tissue and pulmonary edoema caused by pulmonary vascular injury (Shi et al. 2014; Tian et al. 2019). The pathogenesis of ALI is complicated. Various immunomodulators that play critical roles in ALI, such as NO, iNOS, COX-2, IL-1β, IL-6, and TNF-α are regulated by nuclear factor-kappa B (NF-κB) and active IκBα kinase (IKK) signalling pathways (Qiao et al. 2013; Pei et al. 2019; Um et al. 2020). The pro-inflammatory factors such as IL-1β, IL-6 and TNF-α appear in the early phase of inflammatory response and aggravate lung injury (Pei et al. 2019). The anti-inflammatory factors such as IL-4, IL-10 and IL-13 can alleviate lung injury (Wu et al. 2009; Wang et al. 2016). The activation of the complement system and active complement fragments may exacerbate lung injury (Guo and Ward 2005; Sarma and Ward 2011; Bosmann and Ward 2012). In the clinic, the elevation of complement 3a (C3a) and complement 5a (C5a) in bronchoalveolar lavage fluid (BALF) are used as the diagnostic indicator of ALI (Guo and Ward 2005; Bosmann and Ward 2012; Wu et al. 2021). Additionally, oxidative damage can exacerbate lung damage.