Reversible complete heart block in a patient with coronavirus disease 2019.

Patients infected with novel coronavirus (SARS-CoV-2) can present with a variety of arrhythmias. We report an unusual case of reversible complete heart block (CHB) in the setting of acute coronavirus disease 2019 (COVID-19). A 23-year-old male with a history of Hodgkin's Lymphoma presented with dizziness and syncope. He was found to be in CHB associated with hypotension requiring a transvenous pacemaker. Methylprednisolone and remdesivir were started with rapid resolution of the CHB. Further study is needed to determine the mechanism of CHB in COVID-19. This case underscores the importance of including COVID-19 in one's differential diagnosis for acute CHB.

SP-R210 (Myo18A) Isoforms as Intrinsic Modulators of Macrophage Priming and Activation.

The surfactant protein (SP-A) receptor SP-R210 has been shown to increase phagocytosis of SP-A-bound pathogens and to modulate cytokine secretion by immune cells. SP-A plays an important role in pulmonary immunity by enhancing opsonization and clearance of pathogens and by modulating macrophage inflammatory responses. Alternative splicing of the Myo18A gene results in two isoforms: SP-R210S and SP-R210L, with the latter predominantly expressed in alveolar macrophages. In this study we show that SP-A is required for optimal expression of SP-R210L on alveolar macrophages. Interestingly, pre-treatment with SP-A prepared by different methods either enhances or suppresses responsiveness to LPS, possibly due to differential co-isolation of SP-B or other proteins. We also report that dominant negative disruption of SP-R210L augments expression of receptors including SR-A, CD14, and CD36, and enhances macrophages' inflammatory response to TLR stimulation. Finally, because SP-A is known to modulate CD14, we used a variety of techniques to investigate how SP-R210 mediates the effect of SP-A on CD14. These studies revealed a novel physical association between SP-R210S, CD14, and SR-A leading to an enhanced response to LPS, and found that SP-R210L and SP-R210S regulate internalization of CD14 via distinct macropinocytosis-like mechanisms. Together, our findings support a model in which SP-R210 isoforms differentially regulate trafficking, expression, and activation of innate immune receptors on macrophages.