scholarly journals Community-Acquired Respiratory Distress Syndrome Toxin: Unique Exotoxin for M. pneumoniae

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiaoling Su ◽  
Xiaoxing You ◽  
Haodang Luo ◽  
Keying Liang ◽  
Li Chen ◽  
...  
Keyword(s):  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Inflammatory Responses ◽  
Structural Characteristics ◽  
Host Cells ◽  
Cell Swelling ◽  
Chronic Obstructive ◽  
Atypical Pneumonia ◽  
Chronic Obstructive Pulmonary Disorder

Mycoplasma pneumoniae infection often causes respiratory diseases in humans, particularly in children and adults with atypical pneumonia and community-acquired pneumonia (CAP), and is often exacerbated by co-infection with other lung diseases, such as asthma, bronchitis, and chronic obstructive pulmonary disorder. Community-acquired respiratory distress syndrome toxin (CARDS TX) is the only exotoxin produced by M. pneumoniae and has been extensively studied for its ADP-ribosyltransferase (ADPRT) activity and cellular vacuolization properties. Additionally, CARDS TX induces inflammatory responses, resulting in cell swelling, nuclear lysis, mucus proliferation, and cell vacuolization. CARDS TX enters host cells by binding to the host receptor and is then reverse transported to the endoplasmic reticulum to exert its pathogenic effects. In this review, we focus on the structural characteristics, functional activity, distribution and receptors, mechanism of cell entry, and inflammatory response of CARDS TX was examined. Overall, the findings of this review provide a theoretical basis for further investigation of the mechanism of M. pneumoniae infection and the development of clinical diagnosis and vaccines.

Acute respiratory failure and acute respiratory distress syndrome

2018 ◽  
Author(s):  
Luciano Gattinon ◽  
Eleonora Carlesso
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Failure ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Partial Pressure ◽  
Distress Syndrome ◽  
Gas Analysis ◽  
Chronic Obstructive ◽  
Low Oxygen ◽  
Arterial Blood

Respiratory failure (RF) is defined as the acute or chronic impairment of respiratory system function to maintain normal oxygen and CO2 values when breathing room air. ‘Oxygenation failure’ occurs when O2 partial pressure (PaO2) value is lower than the normal predicted values for age and altitude and may be due to ventilation/perfusion mismatch or low oxygen concentration in the inspired air. In contrast, ‘ventilatory failure’ primarily involves CO2 elimination, with arterial CO2 partial pressure (PaCO2) higher than 45 mmHg. The most common causes are exacerbation of chronic obstructive pulmonary disease (COPD), asthma, and neuromuscular fatigue, leading to dyspnoea, tachypnoea, tachycardia, use of accessory muscles of respiration, and altered consciousness. History and arterial blood gas analysis is the easiest way to assess the nature of acute RF and treatment should solve the baseline pathology. In severe cases mechanical ventilation is necessary as a ‘buying time’ therapy. The acute hypoxemic RF arising from widespread diffuse injury to the alveolar-capillary membrane is termed Acute Respiratory Distress Syndrome (ARDS), which is the clinical and radiographic manifestation of acute pulmonary inflammatory states.

scholarly journals Functional promoter variants in sphingosine 1-phosphate receptor 3 associate with susceptibility to sepsis-associated acute respiratory distress syndrome

2013 ◽  
Vol 305 (7) ◽  
pp. L467-L477 ◽  
Author(s):  
Xiaoguang Sun ◽  
Shwu-Fan Ma ◽  
Michael S. Wade ◽  
Marialbert Acosta-Herrera ◽  
Jesús Villar ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Inflammatory Responses ◽  
Case Control ◽  
Nucleotide Polymorphisms ◽  
Mobility Shift ◽  
Protein Levels ◽  
Sphingosine 1 Phosphate

The genetic mechanisms underlying the susceptibility to acute respiratory distress syndrome (ARDS) are poorly understood. We previously demonstrated that sphingosine 1-phosphate (S1P) and the S1P receptor S1PR3 are intimately involved in lung inflammatory responses and vascular barrier regulation. Furthermore, plasma S1PR3 protein levels were shown to serve as a biomarker of severity in critically ill ARDS patients. This study explores the contribution of single nucleotide polymorphisms (SNPs) of the S1PR3 gene to sepsis-associated ARDS. S1PR3 SNPs were identified by sequencing the entire gene and tagging SNPs selected for case-control association analysis in African- and ED samples from Chicago, with independent replication in a European case-control study of Spanish individuals. Electrophoretic mobility shift assays, luciferase activity assays, and protein immunoassays were utilized to assess the functionality of associated SNPs. A total of 80 variants, including 29 novel SNPs, were identified. Because of limited sample size, conclusive findings could not be drawn in African-descent ARDS subjects; however, significant associations were found for two promoter SNPs (rs7022797 −1899T/G; rs11137480 −1785G/C), across two ED samples supporting the association of alleles −1899G and −1785C with decreased risk for sepsis-associated ARDS. In addition, these alleles significantly reduced transcription factor binding to the S1PR3 promoter; reduced S1PR3 promoter activity, a response particularly striking after TNF-α challenge; and were associated with lower plasma S1PR3 protein levels in ARDS patients. These highly functional studies support S1PR3 as a novel ARDS candidate gene and a potential target for individualized therapy.

Acute respiratory failure and acute respiratory distress syndrome

2015 ◽  
Author(s):  
Luciano Gattinon ◽  
Eleonora Carlesso
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Failure ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Partial Pressure ◽  
Distress Syndrome ◽  
Gas Analysis ◽  
Chronic Obstructive ◽  
Low Oxygen ◽  
Arterial Blood

Respiratory failure (RF) is defined as the acute or chronic impairment of respiratory system function to maintain normal oxygen and CO2 values when breathing room air. ‘Oxygenation failure’ occurs when O2 partial pressure (PaO2) value is lower than the normal predicted values for age and altitude and may be due to ventilation/perfusion mismatch or low oxygen concentration in the inspired air. In contrast, ‘ventilatory failure’ primarily involves CO2 elimination, with arterial CO2 partial pressure (PaCO2) higher than 45 mmHg. The most common causes are exacerbation of chronic obstructive pulmonary disease (COPD), asthma, and neuromuscular fatigue, leading to dyspnoea, tachypnoea, tachycardia, use of accessory muscles of respiration, and altered consciousness. History and arterial blood gas analysis is the easiest way to assess the nature of acute RF and treatment should solve the baseline pathology. In severe cases mechanical ventilation is necessary as a ‘buying time’ therapy. The acute hypoxemic RF arising from widespread diffuse injury to the alveolar-capillary membrane is termed Acute Respiratory Distress Syndrome (ARDS), which is the clinical and radiographic manifestation of acute pulmonary inflammatory states.

scholarly journals Differential Redox State and Iron Regulation in Chronic Obstructive Pulmonary Disease, Acute Respiratory Distress Syndrome and Coronavirus Disease 2019

Antioxidants ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1460
Author(s):  
Lorena Duca ◽  
Sara Ottolenghi ◽  
Silvia Coppola ◽  
Rocco Rinaldo ◽  
Michele Dei Cas ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Redox State ◽  
Distress Syndrome ◽  
Iron Regulation ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Hematopoietic Response

In patients affected by Acute Respiratory Distress Syndrome (ARDS), Chronic Obstructive Pulmonary Disease (COPD) and Coronavirus Disease 2019 (COVID-19), unclear mechanisms negatively interfere with the hematopoietic response to hypoxia. Although stimulated by physiological hypoxia, pulmonary hypoxic patients usually develop anemia, which may ultimately complicate the outcome. To characterize this non-adaptive response, we dissected the interplay among the redox state, iron regulation, and inflammation in patients challenged by either acute (ARDS and COVID-19) or chronic (COPD) hypoxia. To this purpose, we evaluated a panel of redox state biomarkers that may integrate the routine iron metabolism assays to monitor the patients’ inflammatory and oxidative state. We measured redox and hematopoietic regulators in 20 ARDS patients, 20 ambulatory COPD patients, 9 COVID-19 ARDS-like patients, and 10 age-matched non-hypoxic healthy volunteers (controls). All the examined pathological conditions induced hypoxia, with ARDS and COVID-19 depressing the hematopoietic response without remarkable effects on erythropoietin. Free iron was higher than the controls in all patients, with higher levels of hepcidin and soluble transferrin receptor in ARDS and COVID-19. All markers of the redox state and antioxidant barrier were overexpressed in ARDS and COVID-19. However, glutathionyl hemoglobin, a candidate marker for the redox imbalance, was especially low in ARDS, despite depressed levels of glutathione being present in all patients. Although iron regulation was dysfunctional in all groups, the depressed antioxidant barrier in ARDS, and to a lesser extent in COVID-19, might induce greater inflammatory responses with consequent anemia.

scholarly journals Developing the nomogram for the prediction of in-hospital incidence of acute respiratory distress syndrome in patients with COVID-19

2020 ◽  
Author(s):  
Ning Ding ◽  
Yang Zhou ◽  
Guifang Yang ◽  
Cuirong Guo ◽  
Fengning Tang ◽  
...  
Keyword(s):  
Risk Factors ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Treatment Plan ◽  
Health Centre ◽  
White Blood Count ◽  
Chronic Obstructive ◽  
Public Health Centre

Abstract Background: Acute respiratory distress syndrome (ARDS) was the most common complication of coronavirus disease-2019(COVID-19), leading to poor clinical outcomes. However, the model to predict the in-hospital incidence of ARDS in patients with COVID-19 is limited. Therefore, we aimed to develop a predictive nomogram for the in-hospital incidence of ARDS in COVID-19 patients.Methods: Patients with COVID-19 admitted to Changsha Public Health Centre between Jan 30, 2020, and Feb 22, 2020, were enrolled. Clinical characteristics and laboratory variables were analyzed in patients with ARDS. Risk factors for ARDS were selected by LASSO binary logistic regression. Nomogram was established based on risk factors and validated by the dataset.Results: A total of 113 patients, involving 99 in the non-ARDS group and 14 in the ARDS group were included in the study. 8 variables including hypertension, chronic obstructive pulmonary disease (COPD), cough, lactate dehydrogenase (LDH), creatine kinase (CK), white blood count (WBC), body temperature, and heart rate were identified to be included in the model. The specificity, sensitivity, and accuracy of the full model were 100%, 85.7%, and 87.5% respectively. The calibration curve also showed good agreement between the predicted and observed values in the model.Conclusions: The nomogram can predict the in-hospital incidence of ARDS in COVID-19 patients. It helps physicians to make an individualized treatment plan for each patient.

Acute Respiratory Distress Syndrome

2005 ◽  
Vol 18 (2) ◽  
pp. 118-131 ◽  
Author(s):  
Brian S. Burleson ◽  
Erik D. Maki
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Inflammatory Responses ◽  
Treatment Options ◽  
Clinical Trial Design ◽  
Severe Form ◽  
Consensus Definition ◽  
Definition Of

Acute lung injury is a syndrome diagnosed clinically and is one of the most common causes of respiratory failure seen in the intensive care unit. A consensus definition of this and its more severe form, acute respiratory distress syndrome (ARDS), has allowed for better consistency in determining the epidemiology and facilitates consistent clinical trial design to better find therapies to treat or prevent it. Patients who present with ARDS usually show signs of tachpnea or dyspnea and have underlying conditions that promote inflammatory responses. The pathogenesis involves an inflammatory insult that eventually destroys the pulmonary capillary vasculature as well as alveoli. Pathophysiologically, the patient with ARDS may progress through as many as 3 phases: exudative, proliferative, and fibrotic. Treatment options can be either nonpharmacologic or pharmacologic and are limited. Ventilator strategies such as low-tidal-volume ventilation have improved outcomes in these patients, while corticosteroid use is not as established to provide morbidity or mortality benefit. Other therapies have been investigated with inconclusive or disappointing results for the treatment of this fatal syndrome.

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