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• COVID-19 has no distinct pathogenesis or effective treatment. • COVID-19 could progress to a stage requiring lung transplant. • Symptoms of patients with COVID-19 may involve mast cell activation. • COVID-19 involves proinflammatory mediators released from mast cells. • A patient with severe COVID-19 improved by addressing mast cell activation. SARS-CoV-2 infects cells, leading to a complex immune response that involves the release of mediators, most of which are released from mast cells, leading to lung edema, fibrosis, inflammation, and microthromboses—hallmarks of COVID-19. Here, we report on a patient who was initially hospitalized with severe COVID-19 pneumonia as well as physical and mental fatigue. Despite having been treated with albuterol, azithromycin, ceftriaxone, convalescent plasma, and dexamethasone, her condition continued to worsen to the extent that she was considered for double lung transplant. Four months after a novel integrative treatment approach that primarily aimed at inhibiting mast cells and their mediators, using rupatadine, famotidine, misoprostol, vitamin D3 luteolin, quercetin, and erythropoietin, the patient recovered fully. [ABSTRACT FROM AUTHOR]

Mast-cell expressed membrane protein-1 (MCEMP1) is higher in patients with idiopathic pulmonary fibrosis (IPF) with an increased risk of death. Here we aimed to establish the mechanistic role of MCEMP1 in pulmonary fibrosis. We identified increased MCEMP1 expression in classical monocytes and alveolar macrophages in IPF compared with controls. MCEMP1 is upregulated by transforming growth factor beta (TGFβ) at the mRNA and protein levels in monocytic leukemia THP-1 cells. TGFβ-mediated MCEMP1 upregulation results from the cooperation of SMAD3 and SP1 via concomitant binding to SMAD3/SP1 cis-regulatory elements within the MCEMP1 promoter. We also found that MCEMP1 regulates TGFb-mediated monocyte chemotaxis, adhesion, and migration. Our results suggest that MCEMP1 may regulate the migration and transition of monocytes to monocyte-derived alveolar macrophages during pulmonary fibrosis development and progression. [ABSTRACT FROM AUTHOR]

B Description: b A 29-year-old female with systemic lupus erythematosus and Group 1 PAH presented as a transfer for lung transplant evaluation due to progressive right ventricular (RV) failure despite therapy with milrinone, remodulin IV, ambrisentan, and sildenafil. B Introduction: b Central cannulations of veno-arterial (VA) extracorporeal membranous oxygenation (ECMO) devices are conventionally associated with post-cardiotomy cardiogenic shock. There are several studies with pumpless lung assist devices or peripherally inserted VA-ECMO as a bridge to transplant in those with pulmonary arterial hypertension (PAH) and shock. [Extracted from the article]