Heme Oxygenase-1 Expression in Dendritic Cells Contributes to Protective Immunity against Herpes Simplex Virus Skin Infection

Herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) infections are highly prevalent in the human population and produce mild to life-threatening diseases. These viruses interfere with the function and viability of dendritic cells (DCs), which are professional antigen-presenting cells that initiat...

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Bibliographic Details
Published in:	Antioxidants Vol. 12; no. 6; p. 1170
Main Authors:	Tognarelli, Eduardo I, Duarte, Luisa F, Farías, Mónica A, Cancino, Felipe A, Corrales, Nicolás, Ibáñez, Francisco J, Riedel, Claudia A, Bueno, Susan M, Kalergis, Alexis M, González, Pablo A
Format:	Journal Article
Language:	English
Published:	Switzerland MDPI AG 29-05-2023 MDPI
Subjects:	adaptive response Antibodies Antigen presentation Antigen-presenting cells Antiviral activity antiviral drug Apoptosis Bone marrow Carbon monoxide CD4 antigen Cell activation Cloning Cytokines Dendritic cells Drinking water Enzymes Epithelial cells Health aspects Helper cells Heme Heme oxygenase (decyclizing) heme oxygenase-1 Herpes simplex Herpes simplex virus Herpes viruses Infection Infections Inflammation Interleukin 10 Lymphocytes Lymphocytes T Medical research Medicine, Experimental Oxygenase Peptides Phenotypes Proteins Skin skin infection T cell receptors T cells Tetracycline Tetracyclines Viability Viruses California United States > US herpes simplex virus adaptive response dendritic cells antiviral drug skin infection Treg Treg/Th17 heme oxygenase-1 Th17
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Summary:	Herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) infections are highly prevalent in the human population and produce mild to life-threatening diseases. These viruses interfere with the function and viability of dendritic cells (DCs), which are professional antigen-presenting cells that initiate and regulate the host's antiviral immune responses. Heme oxygenase-1 (HO-1) is an inducible host enzyme with reported antiviral activity against HSVs in epithelial cells and neurons. Here, we sought to assess whether HO-1 modulates the function and viability of DCs upon infection with HSV-1 or HSV-2. We found that the stimulation of HO-1 expression in HSV-inoculated DCs significantly recovered the viability of these cells and hampered viral egress. Furthermore, HSV-infected DCs stimulated to express HO-1 promoted the expression of anti-inflammatory molecules, such as PDL-1 and IL-10, and the activation of virus-specific CD4 T cells with regulatory (Treg), Th17 and Treg/Th17 phenotypes. Moreover, HSV-infected DCs stimulated to express HO-1 and then transferred into mice, promoted the activation of virus-specific T cells and improved the outcome of HSV-1 skin infection. These findings suggest that stimulation of HO-1 expression in DCs limits the deleterious effects of HSVs over these cells and induces a favorable virus-specific immune response in the skin against HSV-1.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	2076-3921 2076-3921
DOI:	10.3390/antiox12061170