Clinical Features and Outcomes of Severe Acute Respiratory Syndrome and Predictive Factors for Acute Respiratory Distress Syndrome

Chen, Cheng-Yu; Lee, Chen‐Hsen; Liu, Cheng-Yi; Wang, Jia-Horng; Wang, Lee-Min; Perng, Reury-Perng

doi:10.1016/s1726-4901(09)70124-8

“…ALI and its more severe form, ARDS, are devastating end-stage lung diseases that can arise following a variety of acute insults to the lung epithelium and occur frequently following infection with SARS-CoV and H5N1 and H1N1 influenza viruses in humans (11, 43, 44). Despite significant advances in treatment options, the overall mortality rates remain substantial and range between 30 and 60%, resulting in ~75,000 deaths in the United States and over a million deaths globally each year (45).…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of Severe Acute Respiratory Syndrome Coronavirus-Induced Acute Lung Injury

Gralinski

¹

,

Bankhead

²

,

Jeng

³

et al. 2013

mBio

View full text Add to dashboard Cite

Systems biology offers considerable promise in uncovering novel pathways by which viruses and other microbial pathogens interact with host signaling and expression networks to mediate disease severity. In this study, we have developed an unbiased modeling approach to identify new pathways and network connections mediating acute lung injury, using severe acute respiratory syndrome coronavirus (SARS-CoV) as a model pathogen. We utilized a time course of matched virologic, pathological, and transcriptomic data within a novel methodological framework that can detect pathway enrichment among key highly connected network genes. This unbiased approach produced a high-priority list of 4 genes in one pathway out of over 3,500 genes that were differentially expressed following SARS-CoV infection. With these data, we predicted that the urokinase and other wound repair pathways would regulate lethal versus sublethal disease following SARS-CoV infection in mice. We validated the importance of the urokinase pathway for SARS-CoV disease severity using genetically defined knockout mice, proteomic correlates of pathway activation, and pathological disease severity. The results of these studies demonstrate that a fine balance exists between host coagulation and fibrinolysin pathways regulating pathological disease outcomes, including diffuse alveolar damage and acute lung injury, following infection with highly pathogenic respiratory viruses, such as SARS-CoV.

show abstract

“…The severity of lymphopenia is correlated with the severity of lung injury [94,97]. The autopsy findings of severe ARDS patients and experimental animals infected with influenza viruses show lymphocyte depletion of whole lymphoid tissues [98].…”

Section: Treatmentmentioning

confidence: 99%

Pneumonia, Acute Respiratory Distress Syndrome, and Early Immune-Modulator Therapy

Lee

¹

2017

IJMS

View full text Add to dashboard Cite

Acute respiratory distress syndrome (ARDS) is caused by infectious insults, such as pneumonia from various pathogens or related to other noninfectious events. Clinical and histopathologic characteristics are similar across severely affected patients, suggesting that a common mode of immune reaction may be involved in the immunopathogenesis of ARDS. There may be etiologic substances that have an affinity for respiratory cells and induce lung cell injury in cases of ARDS. These substances originate not only from pathogens, but also from injured host cells. At the molecular level, these substances have various sizes and biochemical characteristics, classifying them as protein substances and non-protein substances. Immune cells and immune proteins may recognize and act on these substances, including pathogenic proteins and peptides, depending upon the size and biochemical properties of the substances (this theory is known as the protein-homeostasis-system hypothesis). The severity or chronicity of ARDS depends on the amount of etiologic substances with corresponding immune reactions, the duration of the appearance of specific immune cells, or the repertoire of specific immune cells that control the substances. Therefore, treatment with early systemic immune modulators (corticosteroids and/or intravenous immunoglobulin) as soon as possible may reduce aberrant immune responses in the potential stage of ARDS.

show abstract

“…Lymphopenia may be characteristic of severe pneumonia patients infected with respiratory pathogens, including influenza viruses, corona viruses, the measles virus, and M. pneumoniae [94][95][96][97]. The severity of lymphopenia is correlated with the severity of lung injury [94,97].…”

Section: Treatmentmentioning

confidence: 99%

“…The severity of lymphopenia is correlated with the severity of lung injury [94,97]. The autopsy findings of severe ARDS patients and experimental animals infected with influenza viruses show lymphocyte depletion of whole lymphoid tissues [98].…”

Section: Treatmentmentioning

confidence: 99%

Pneumonia, Acute Respiratory Distress Syndrome and Early Immune-Modulator Therapy

Lee¹

2016

Preprint

View full text Add to dashboard Cite

Acute respiratory distress syndrome (ARDS) is caused by infectious insults, such as pneumonia from various pathogens or related to other noninfectious events. Clinical and histopathologic characteristics are similar across severely affected patients, suggesting that a common mode of immune reaction may be involved in the immunopathogenesis of ARDS. There may be etiologic substances that have an affinity for respiratory cells and induce lung cell injury in cases of ARDS. These substances originate not only from pathogens, but also from injured host cells. At the molecular level, these substances have various sizes and biochemical characteristics, classifying them as protein substances and non-protein substances. Immune cells and immune proteins may recognize and act on these substances, including pathogenic proteins and peptides, depending upon the size and biochemical properties of the substances (this theory is known as the protein-homeostasis-system hypothesis). The severity or chronicity of ARDS depends on the amount of etiologic substances with corresponding immune reactions, the duration of the appearance of specific immune cells, or the repertoire of specific immune cells that control the substances. Therefore, treatment with early systemic immune modulators (corticosteroids and/or intravenous immunoglobulin) as soon as possible may reduce aberrant immune responses in the potential stage of ARDS.

show abstract

Clinical Features and Outcomes of Severe Acute Respiratory Syndrome and Predictive Factors for Acute Respiratory Distress Syndrome

Abstract: The clinical manifestations of SARS showed high variability, and were related to the underlying health status of individual patients. Importantly, the development of ARDS was associated with significant mortality, despite aggressive therapy.

Cited by 94 publications

References 16 publications

Mechanisms of Severe Acute Respiratory Syndrome Coronavirus-Induced Acute Lung Injury

Mechanisms of Severe Acute Respiratory Syndrome Coronavirus-Induced Acute Lung Injury

Pneumonia, Acute Respiratory Distress Syndrome, and Early Immune-Modulator Therapy

Pneumonia, Acute Respiratory Distress Syndrome and Early Immune-Modulator Therapy

Contact Info

Product

Resources

About