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American Journal of Respiratory and Critical Care Medicine ; 205(1), 2022.
Article in English | EMBASE | ID: covidwho-1927902

ABSTRACT

Introduction: Dexamethasone decreases mortality in patients with severe COVID-19. The effects of dexamethasone on inflammation and repair in patients with severe COVID-19 are not well understood. We integrated tracheal aspirate (TA) and peripheral blood bulk/single-cell RNA sequencing to study the effect of dexamethasone on patients with COVID-19 ARDS. Methods: We studied selected patients from a cohort of adults with COVID-19 admitted to three hospitals in San Francisco, California from April 2020 to February 2021. Immunosuppression was not used to treat COVID-19 ARDS at these hospitals prior to July 2020, but was routinely used in these patients after this date. For this analysis, we included patients who were mechanically ventilated for COVID-19 ARDS for whom sequencing samples were available within four days of intubation. We excluded patients who received steroids prior to July 2020, subjects who received immunosuppression other than dexamethasone (e.g., tocilizumab) prior to sample collection, and chronically immunosuppressed subjects. We compared bulk RNASeq from TA and single cell RNASeq from TA and whole blood from subjects who received dexamethasone to subjects who did not receive dexamethasone. In addition, we studied the effect of dexamethasone on peripheral blood cytokine concentrations to confirm the effects of observed changes in gene expression. Results: TA bulk RNASeq was available from 20 subjects (six dexamethasone, 14 non-dexamethasone). There was no significant difference in age, sex, smoking, or BMI between groups. After correcting for multiple comparisons, 947 genes were differentially expressed in TA from subjects who received dexamethasone. Ingenuity Pathway Analysis predicted decreased activation of interferon, JAK/STAT, and NLRP12 signaling in subjects who received dexamethasone (Figure 1A). TA scRNASeq samples were available from ten dexamethasone-treated subjects and nine non-dexamethasone subjects. Whole blood scRNAseq samples were available for seven dexamethasone and eight non-dexamethasone subjects (Figure 1B). Eight subjects (three treated with dexamethasone) had both TA and whole blood scRNAseq samples available for analysis. Dexamethasone had distinct effects on the proportions of immune cells in tracheal aspirates and whole blood (Figure 1C). In 36 dexamethasone vs 42 non-dexamethasone subjects, treatment with dexamethasone was associated with significantly increased concentrations of IL-10 and decreased concentrations of IL-6 (Figure 1D). Conclusions: Dexamethasone decreases pro-inflammatory gene expression in the respiratory tract and peripheral blood of patients with COVID-19 ARDS. The effect of dexamethasone on specific cell populations may be distinct in the respiratory tract and peripheral blood.

2.
Journal of Livestock Science ; 12:213-219, 2021.
Article in English | Web of Science | ID: covidwho-1296395

ABSTRACT

In late December 2019, Wuhan city of Hubei province, China faced a newly emerged highly contagious viral zoonosis mainly characterized by respiratory illness, associated with pneumonia of unknown etiology which claimed many lives. The virus was then provisionally designated as 2019-nCoV by WHO and officially named as Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) by International Committee on Taxonomy of Viruses (ICTV). On 11 Feb 2020, WHO officially announced the name of disease as Coronavirus disease 2019 (COVID-19) and declared the global pandemic on March 11, 2020. Initially, the disease was highly restricted to China but later it scared the world because hugenumber of new cases was reported from the entire world in a short period of 5 months. The dynamic spread of this contagious virus occurred due to exposure of individuals from infected aerosols, community contact and travelling of affected individual worldwide. Bats were thought to be the initial source of this pandemic but the intermediate host of this zoonosis is yet to be established. Many studies reported fever, dry cough, dyspnea, generalized weakness, anosmia, ageusia, muscle ache, rhinorrhea, headache, nausea, conjunctivitis, vomiting and diarrhoea along with many non-specific symptoms as clinical signs of the disease. Many treatment regimen including various antivirals, antibiotics, neutralizing antibodies, repurposed drugs and traditional medicines were being explored but the authorized effective treatment regimen is still awaited. This review is aimed to summarize the current scenario and status of probable treatment options available for ongoing illness caused by the novel coronavirus.

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