TNFα Blockade Inhibits Both Initial and Continued Control of Pulmonary Coccidioides
AffiliationValley Fever Center for Excellence, University of Arizona
Department of Immunobiology, University of Arizona
Department of Medicine, University of Arizona
MetadataShow full item record
PublisherFrontiers Media S.A.
CitationPowell, D. A., Shubitz, L. F., Butkiewicz, C. D., Trinh, H. T., Donovan, F. M., Frelinger, J. A., & Galgiani, J. N. (2022). TNFα Blockade Inhibits Both Initial and Continued Control of Pulmonary Coccidioides. Frontiers in Cellular and Infection Microbiology.
RightsCopyright © 2022 Powell, Shubitz, Butkiewicz, Trinh, Donovan, Frelinger and Galgiani. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY).
Collection InformationThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at firstname.lastname@example.org.
AbstractTumor necrosis factor alpha (TNFα) is a pluripotent cytokine that is important in many infections, though its role in Coccidioides infection remains poorly understood. The need to understand TNFα in Coccidioides infection has increased recently with the widespread use of TNFα inhibitors for a wide variety of autoimmune conditions. Here, we couple the newly developed Coccidioides infection model using strain Cp1038 and C57BL/6 × DBA/2J F1 (B6D2F1) mice. B6D2F1 mice develop long-lasting control of Cp1038. Treatment of B6D2F1 mice with anti-TNFα antibodies permits significant fungal proliferation and death. Additionally, we show that antibody treatment limited to the first 2 weeks of infection was sufficient to induce this same loss of fungal control. Importantly, anti-TNFα antibody treatment initiated after fungal control leads to a loss of host control. These results highlight the importance of TNFα in both the initial control of murine Coccidioides and ongoing suppression of the fungal disease. Copyright © 2022 Powell, Shubitz, Butkiewicz, Trinh, Donovan, Frelinger and Galgiani.
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VersionFinal published version
Except where otherwise noted, this item's license is described as Copyright © 2022 Powell, Shubitz, Butkiewicz, Trinh, Donovan, Frelinger and Galgiani. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY).
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