Tetracycline to Limit the Innate Immune Response in Acute Respiratory Distress Syndrome

2019 ◽  
Author(s):  
Keyword(s):  
Immune Response ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Innate Immune Response ◽  
Distress Syndrome ◽  
Innate Immune

scholarly journals Early Upregulation of Acute Respiratory Distress Syndrome-Associated Cytokines Promotes Lethal Disease in an Aged-Mouse Model of Severe Acute Respiratory Syndrome Coronavirus Infection

2009 ◽  
Vol 83 (14) ◽  
pp. 7062-7074 ◽  
Author(s):  
Barry Rockx ◽  
Tracey Baas ◽  
Gregory A. Zornetzer ◽  
Bart Haagmans ◽  
Timothy Sheahan ◽  
...  
Keyword(s):  
Immune Response ◽  
Acute Respiratory Distress Syndrome ◽  
Severe Acute Respiratory Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Host Response ◽  
Molecular Mechanisms ◽  
Distress Syndrome ◽  
Aged Mice ◽  
Young Mice

ABSTRACT Several respiratory viruses, including influenza virus and severe acute respiratory syndrome coronavirus (SARS-CoV), produce more severe disease in the elderly, yet the molecular mechanisms governing age-related susceptibility remain poorly studied. Advanced age was significantly associated with increased SARS-related deaths, primarily due to the onset of early- and late-stage acute respiratory distress syndrome (ARDS) and pulmonary fibrosis. Infection of aged, but not young, mice with recombinant viruses bearing spike glycoproteins derived from early human or palm civet isolates resulted in death accompanied by pathological changes associated with ARDS. In aged mice, a greater number of differentially expressed genes were observed than in young mice, whose responses were significantly delayed. Differences between lethal and nonlethal virus phenotypes in aged mice could be attributed to differences in host response kinetics rather than virus kinetics. SARS-CoV infection induced a range of interferon, cytokine, and pulmonary wound-healing genes, as well as several genes associated with the onset of ARDS. Mice that died also showed unique transcriptional profiles of immune response, apoptosis, cell cycle control, and stress. Cytokines associated with ARDS were significantly upregulated in animals experiencing lung pathology and lethal disease, while the same animals experienced downregulation of the ACE2 receptor. These data suggest that the magnitude and kinetics of a disproportionately strong host innate immune response contributed to severe respiratory stress and lethality. Although the molecular mechanisms governing ARDS pathophysiology remain unknown in aged animals, these studies reveal a strategy for dissecting the genetic pathways by which SARS-CoV infection induces changes in the host response, leading to death.

scholarly journals Tempering Macrophage plasticity for controlling SARS-CoV-2 infection for managing COVID-19 disease

2020 ◽  
Author(s):  
Devinder Toor ◽  
Aklank Jain ◽  
Shivani Kalhan ◽  
Harmesh Manocha ◽  
Vivek Kumar Sharma ◽  
...  
Keyword(s):  
Immune Response ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Failure ◽  
Pulmonary Fibrosis ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Antiviral Immune Response ◽  
Macrophage Plasticity

Hyper activation of macrophages contributes to acute respiratory distress syndrome, respiratory failure, and subsequent death of COVID-19 cases. Given this, tempering macrophage plasticity is paramount and the highest priority for the management of COVID-19 cases. In this context we here propose that either exchange or in situ re-programming of derailed Th17+ alveolar macrophages/ Slan+ DC with Th1 programmed counterpart would potentially mitigate or abolish pulmonary fibrosis. This approach is also anticipated to afford antiviral immune response and promote recovery in the patients and hold tremendous potential for managing severely infected patients by both curbing viruses and enhancing post-treatment recovery.

scholarly journals Functional alteration of innate T cells in critically ill Covid-19 patients

2020 ◽  
Author(s):  
Youenn Jouan ◽  
Antoine Guillon ◽  
Loïc Gonzalez ◽  
Yonatan Perez ◽  
Stephan Ehrmann ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Critically Ill ◽  
Distress Syndrome ◽  
Potential Contribution ◽  
Innate T Cells ◽  
Functional Alteration

AbstractCovid-19 can induce lung infection ranging from mild pneumonia to life-threatening acute respiratory distress syndrome (ARDS). Dysregulated host immune response in the lung is a key feature in ARDS pathophysiology. However, cellular actors in Covid-19-driven ARDS are poorly understood. Here, we dynamically analyzed the biology of innate T cells, a heterogeneous class (MAIT, γδT and iNKT cells) of T lymphocytes, presenting potent anti-infective and regulatory functions. Patients presented a compartmentalized lung inflammation paralleled with a limited systemic inflammation. Circulating innate T cells of critically ill Covid-19 patients presented a profound and persistent phenotypic and functional alteration. Highly activated innate T cells were detected in airways of patients suggesting a recruitment to the inflamed site and a potential contribution in the regulation of the local inflammation. Finally, the expression of the CD69 activation marker on blood iNKT and MAIT cells at inclusion was predictive of disease severity. Thus, patients present an altered innate T cell biology that may account for the dysregulated immune response observed in Covid-19-related acute respiratory distress syndrome.

Rituximab Administration in Coronavirus Pandemic Era: A Mini-Review of Clinical Evidence

2021 ◽  
Author(s):  
Ahmad Shamabadi ◽  
Hamidreza Mahmoudi ◽  
Maryam Daneshpazhooh
Keyword(s):  
Immune Response ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Cohort Studies ◽  
B Cell ◽  
Clinical Evidence ◽  
Distress Syndrome ◽  
Insufficient Evidence ◽  
High Quality

Rituximab (RTX), as a B cell-depleting agent, is indicated in treating several malignancies and autoimmune diseases. The management of patients currently receiving RTX and patients starting the medication raised concerns in the pandemic era. Theoretically, suppressing the immune response at the beginning of coronavirus disease 2019 (COVID-19) enhances viral replication, but it prevents acute respiratory distress syndrome as the disease progresses. This review aims to investigate the results of RTX administration in patients during the pandemic era. There is insufficient evidence to definitively conclude on the safety of RTX during the pandemic. For this purpose, high-quality controlled cohort studies, as well as registry-based studies, would be helpful.

The chance of COVID-19 infection after vaccination

2022 ◽  
Vol 22 ◽  
Author(s):  
Ghazaleh Khalili-Tanha ◽  
Majid Khazaei ◽  
Saman Soleimanpour ◽  
Gordon A Ferns ◽  
Amir Avan
Keyword(s):  
Genetic Diversity ◽  
Immune Response ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Mild Form ◽  
The World ◽  
New Generation ◽  
Pathogenic Infection

Abstract: The outbreak of COVID-19 that began in Wuhan, China, has constituted a new emerging epidemic that has spread around the world. There are some reports on illustrated the patients getting reinfected after recovering from COVID-19. Here we provide an overview of the biphasic cycle of COVID-19, genetic diversity, immune response and chance of reinfection after recovering from COVID-19. The new generation of COVID-19 is highly contagious and pathogenic infection can lead to acute respiratory distress syndrome. Whilst most patients suffer from a mild form of the disease, there is a rising concern that patients who recover from COVID-19 may be at risk of reinfection. The proportion of the infected population, is increasing worldwide; meanwhile, the rate and concern of reinfection by the recovered population are still high. Moreover, there are a few evidence on the chance of COVID-19 infection even after vaccination, which is around one per cent or less. Although the hypothesis of zero reinfections after vaccination has not been clinically proven, further studies should be performed on the recovered class in clusters to study the progression of the exposed with the re-exposed subpopulations to estimate the possibilities of reinfection and, thereby, advocate the use of these antibodies for vaccine creation.

scholarly journals From sepsis to acute respiratory distress syndrome (ARDS): emerging preventive strategies based on molecular and genetic researches

2020 ◽  
Vol 40 (5) ◽  
Author(s):  
Qinghe Hu ◽  
Cuiping Hao ◽  
Sujuan Tang
Keyword(s):  
Immune Response ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Inflammatory Responses ◽  
Systemic Infection ◽  
Immunological Mechanism ◽  
Diagnostic Strategies ◽  
Immunological Mechanisms

Abstract A healthy body activates the immune response to target invading pathogens (i.e. viruses, bacteria, fungi, and parasites) and avoid further systemic infection. The activation of immunological mechanisms includes several components of the immune system, such as innate and acquired immunity. Once any component of the immune response to infections is aberrantly altered or dysregulated, resulting in a failure to clear infection, sepsis will develop through a pro-inflammatory immunological mechanism. Furthermore, the severe inflammatory responses induced by sepsis also increase vascular permeability, leading to acute pulmonary edema and resulting in acute respiratory distress syndrome (ARDS). Apparently, potential for improvement exists in the management of the transition from sepsis to ARDS; thus, this article presents an exhaustive review that highlights the previously unrecognized relationship between sepsis and ARDS and suggests a direction for future therapeutic developments, including plasma and genetic pre-diagnostic strategies and interference with proinflammatory signaling.

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