Aerosol-generating procedures in the office represent a major concern for health care–associated infection of patients and health care providers by SARS-CoV-2, the causative agent for coronavirus disease 2019 (COVID-19). Although the Centers for Disease Control and Prevention has not yet provided any recommendations for the use of portable air purifiers, air purifiers with high-efficiency particulate air (HEPA) filters have been discussed as an adjunctive means for decontamination of SARS-CoV-2 aerosols in health care settings. This commentary discusses HEPA filter mechanisms of action, decontamination time based on efficiency and flow rate, theoretical application to SARS-CoV-2, and limitations. HEPA filter functionality and prior guidance from the Centers for Disease Control and Prevention for SARS-CoV-1 suggest theoretical efficacy for HEPA filters to decontaminate airborne SARS-CoV-2, although direct studies for SARS-CoV-2 have not been performed. Any portable HEPA purifier utilization for SARS-CoV-2 should be considered an adjunctive infection control measure and undertaken with knowledge of HEPA filter functionality and limitations in mind.
Monokine induced by IFN-γ (MIG; CXC chemokine ligand (CXCL)9) is important in T lymphocyte recruitment in organ transplantation. However, it is not known whether this chemokine, in addition to its chemotactic properties, exerts any effect on T lymphocyte effector functions. For in vivo studies, we used a previously characterized murine model of chronic rejection. The recipient mice were treated with anti-MIG/CXCL9 Ab; graft-infiltrating cells were analyzed for IFN-γ production. For in vitro studies, exogenous CXCR3 ligands were added to CD4 lymphocytes in MLRs, and the proliferative responses were measured. Separate experiments quantitated the number of IFN-γ-producing cells in MLRs by ELISPOT. Neutralization of MIG/CXCL9, in the in vivo model, resulted in significant reduction in the percentage of IFN-γ-producing graft-infiltrating T lymphocytes. In vitro experiments demonstrated that 1) exogenous MIG/CXCL9 stimulated CD4 lymphocyte proliferation in a MHC class II-mismatched MLR, 2) MIG/CXCL9 also increased the number of IFN-γ-producing CD4 lymphocytes in ELISPOT, 3) neutralization of MIG/CXCL9 in MLR reduced T lymphocyte proliferation, 4) IFN-γ-inducible protein 10/CXCL10 and IFN-inducible T cell α chemoattractant/CXCL11 had similar effects on T lymphocyte proliferation, 5) MIG/CXCL9 stimulated T lymphocyte proliferation in MHC class I- and total MHC-mismatched MLRs, 6) neutralization of CXCR3 reduced MIG/CXCL9-induced T lymphocyte proliferation and the number of IFN-γ-positive spots on ELISPOT, and 7) the proliferative effects of MIG/CXCL9 were mediated via an IL-2-independent pathway and were controlled by IFN-γ. This study demonstrates that MIG/CXCL9 stimulates T lymphocyte proliferation and effector cytokine production, in addition to its chemotactic effects. This novel observation expands our current understanding of MIG/CXCL9 biology beyond that of mediating T cell trafficking.
The use of topical CE is safe when performing endoscopic endonasal procedures. CE was not associated with any intraoperative complications. The profound intraoperative vasoconstriction does not confer a higher rate of postoperative rebound epistaxis.
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