Quantification of Cytokine Storms During Virus Infections

Yuan, Shu; Jiang, Si‐Cong; Zhang, Zhongwei; Fu, Yu‐Fan; Hu, Jing; Li, Zi-Lin

doi:10.3389/fimmu.2021.659419

Cited by 47 publications

(61 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast, airspace IFN-γ spiked dramatically between 5 and 7 dpi, in concert with the wave of lymphocytic inflammation (Figure 1e) and increasing alveolar-capillary barrier permeability (Figure 1f). These patterns of cytokine expression mimic those seen in patients suffering from severe viral illness, as detailed in a recent review (Yuan et al, 2021). As expected, the neutrophil chemokine KC (Figure 2e) and the monocyte/lymphocyte chemokine MCP-1 (Figure 2f) roughly…”

Section: Airspace Inflammatory Cytokines and Chemokines Parallel The Waves Of Cellular Inflammationsupporting

confidence: 80%

Delayed angiopoietin‐2 blockade reduces influenza‐induced lung injury and improves survival in mice

Gotts

Maishan

Chun

et al. 2021

Physiological Reports

View full text Add to dashboard Cite

Influenza remains a major cause of death and disability with limited treatment options. Studies of acute lung injury have identified angiopoietin‐2 (Ang‐2) as a key prognostic marker and a potential mediator of Acute respiratory distress syndrome. However, the role of Ang‐2 in viral pneumonia remains poorly defined. This study characterized the time course of lung Ang‐2 expression in severe influenza pneumonia and tested the therapeutic potential of Ang‐2 inhibition. We inoculated adult mice with influenza A (PR8 strain) and measured angiopoietin‐1 (Ang‐1), Ang‐2, and Tie2 expressions during the evolution of inflammatory lung injury over the first 7 days post‐infection (dpi). We tested a peptide‐antibody inhibitor of Ang‐2, L1‐7, administered at 2, 4, and 6 dpi and measured arterial oxygen saturation, survival, pulmonary edema, inflammatory cytokines, and viral load. Finally, we infected primary human alveolar type II epithelial (AT2) cells grown in air‐liquid interface culture with influenza and measured Ang‐2 RNA expression. Influenza caused severe lung injury between 5 and 7 dpi in association with increased Ang‐2 lung RNA and a dramatic increase in Ang‐2 protein in bronchoalveolar lavage. Inhibition of Ang‐2 improved oxygenation and survival and reduced pulmonary edema and alveolar‐capillary barrier permeability to protein without major effects on inflammation or viral load. Finally, influenza increased the expression of Ang‐2 RNA in human AT2 cells. The increased Ang‐2 levels in the airspaces during severe influenza pneumonia and the improvement in clinically relevant outcomes after Ang‐2 antagonism suggest that the Ang‐1/Ang‐2 Tie‐2 signaling axis is a promising therapeutic target in influenza and potentially other causes of viral pneumonia.

show abstract

Section: Airspace Inflammatory Cytokines and Chemokines Parallel The Waves Of Cellular Inflammationsupporting

confidence: 80%

Delayed angiopoietin‐2 blockade reduces influenza‐induced lung injury and improves survival in mice

Gotts

Maishan

Chun

et al. 2021

Physiological Reports

View full text Add to dashboard Cite

show abstract

“…These include direct renal injury in the presence of acute tubular necrosis, inflammation, and cytokine storm. A study measuring cytokine storm through various viral infections showed that H1N1 infection increased the number of cytokines compared to COVID-19 [23] . Therefore, COVID-19 induces greater elevation of cytokines, resulting in a more severe disease with the risk of morbidity and/or mortality.…”

Section: Discussionmentioning

confidence: 99%

COVID-19 induced renal injury differs from that in other viral-infections

Parise

Govindarajulu

Ramesh

et al. 2021

Emergency and Critical Care Medicine

View full text Add to dashboard Cite

Background:Kidney injuries caused by several viral diseases have been reported worldwide among all age groups, races, and genders. Of particular importance is coronavirus disease 2019 (COVID-19), and its prevalence in communities infecting all patient populations with symptoms ranging from asymptomatic to severe, including complications and mortality.Methods:Data were acquired from PubMed, Scopus, Google Scholar, Centers for Disease Prevention and Control (CDC), and Lexi-Comp using the following search terms: “COVID-19 and renal pathology,” “COVID-19 induced kidney disease,” “Viral infection induced kidney disease,” and “Viral infection induced renal damage.” Titles and abstracts were manually analyzed as per the exclusion and inclusion criteria of relevant articles; relevance of articles included studies on the pathology of a specific viral infection and the impact of the virus on the adult renal system.Results:The mechanisms for renal disease due to COVID-19 include direct renal tubular injury, cytokine storm, inflammation, thrombosis vs. acute tubular necrosis, thrombotic events, and direct renal injury. Although some mechanisms behind renal dysfunction among the studied viral infections are similar, the prevalence rates of kidney injury or damage differ. This might be described by recommended prophylactic and therapeutic approaches that can alter the viral infection characteristics and possibly the impact a particular organ system.Conclusion:The patient population at risk was old in age and had a high body mass index. The mechanisms associated with renal dysfunction are similar, including direct renal injury through angiotensin converting enzyme 2 (ACE2) entry, inflammation, and thrombosis. The renal pathology of coronaviruses that differs from that of other prevalent viral infections is the activation of cytokine storm, which causes elevations of a greater number and different kinds of cytokines than other viral infections.

show abstract

“…Besides ventilation-perfusion mismatch, intravascular coagulation and alveolar edema, COVID-19 ARDS is a very complex disease, with intrapulmonary shunting, impaired lung diffusion, inflammation, etc. [103][104][105][106][107][108][109]. We cannot expect that early oxygen therapy and pulmonary edema treatments can prevent every COVID-19 patient from the development of ARDS.…”

Section: Clinical Outlookmentioning

confidence: 99%

The Role of Alveolar Edema in COVID-19

Yuan

Jiang

Zhang

et al. 2021

Cells

Self Cite

View full text Add to dashboard Cite

The coronavirus disease 2019 (COVID-19) has spread over the world for more than one year. COVID-19 often develops life-threateninghypoxemia. Endothelial injury caused by the viral infection leads to intravascular coagulation and ventilation–perfusion mismatch. However, besides above pathogenic mechanisms, the role of alveolar edema in the disease progression has not been discussed comprehensively. Since the exudation of pulmonary edema fluid was extremely serious in COVID-19 patients, we bring out a hypothesis that severity of alveolar edema may determine the size of poorly-ventilated area and the blood oxygen content. Treatments to pulmonary edema (conservative fluid management, exogenous surfactant replacementsand ethanol–oxygen vapor therapyhypothetically) may be greatly helpful for reducingthe occurrences of severe cases. Given that late mechanical ventilation may causemucus (edema fluid) to be blown deep intothe small airways,oxygentherapy should be given at the early stages. Theoptimaltimeand blood oxygen saturation (SpO2) thresholdforoxygentherapy are also discussed.

show abstract

Quantification of Cytokine Storms During Virus Infections

Cited by 47 publications

References 36 publications

Delayed angiopoietin‐2 blockade reduces influenza‐induced lung injury and improves survival in mice

Delayed angiopoietin‐2 blockade reduces influenza‐induced lung injury and improves survival in mice

COVID-19 induced renal injury differs from that in other viral-infections

The Role of Alveolar Edema in COVID-19

Contact Info

Product

Resources

About