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IL-13 induced inflammation increases DPP4 abundance but does not enhance MERS-CoV replication in airway epithelia
Journal article   Open access   Peer reviewed

IL-13 induced inflammation increases DPP4 abundance but does not enhance MERS-CoV replication in airway epithelia

Kun Li, Jennifer A Bartlett, Christine L Wohlford-Lenane, Biyun Xue, Andrew L Thurman, Thomas M Gallagher, Alejandro A Pezzulo and Paul B McCray Jr
The Journal of infectious diseases, Vol.229(5), pp.1419-1429
09/12/2023
DOI: 10.1093/infdis/jiad383
PMCID: PMC11095549
PMID: 37698016
url
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11095549View
Published (Version of record) Open Access

Abstract

Background Chronic pulmonary conditions such as asthma and COPD increase the risk of morbidity and mortality during infection with the Middle East respiratory syndrome coronavirus (MERS-CoV). We hypothesized that individuals with such comorbidities are more susceptible to MERS-CoV infection due to increased expression of its receptor, dipeptidyl peptidase 4 (DPP4). Methods We modeled chronic airway disease by treating primary human airway epithelia with the Th2 cytokine IL-13, examining how this impacted DPP4 protein levels along with MERS-CoV entry and replication. Results IL-13 exposure for 3 days led to increased DPP4 protein abundance, while a 21-day treatment increased DPP4 levels and caused goblet cell metaplasia. Surprisingly, despite this increase in receptor availability, MERS-CoV entry and replication were not significantly impacted by IL-13 treatment. Conclusions Our results suggest that increased DPP4 abundance is likely not the primary mechanism leading to increased MERS severity in the setting of Th2 inflammation. Transcriptional profiling analysis highlighted the complexity of IL-13 induced changes in airway epithelia, including altered expression of genes involved in innate immunity, antiviral responses, and maintenance of the extracellular mucus barrier. These data suggest that additional factors likely interact with DPP4 abundance to determine MERS-CoV infection outcomes.

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