Gene expression profiles of nasal epithelium in long COVID and post-COVID

Recent studies suggest that chronic inflammation and immune dysregulation in the local tissues and systemically play a critical role in the pathophysiology of long COVID. Here, we report a role for nasal epithelium in mediating inflammation in a subset of long COVID patients. We demonstrate impaired barrier function of nasal epithelial cells, inadequate wound healing potential, and nasal cell hypersensitivity along with a persistent inflammatory state in long COVID. These inflamed structural cells activate type 1 innate lymphoid cells in the blood of long COVID patients and propagate systemic inflammation. We demonstrated the importance of understanding the immunological mechanisms driving long COVID to develop effective treatments. We highlight the critical role of the nasal epithelial barrier and the interplay between epithelial cells and ILCs in maintaining mucosal homeostasis and contributing to chronic inflammation in long COVID. Overall design: In this study, we examined whether the crosstalk between the nasal epithelium and pro-inflammatory innate lymphoid cells plays a role in modulating the pathophysiology of long COVID. Considering the transcriptome, we studied the functional and phenotypic consequences of dysregulated gene expression patterns, we performed bulk RNA-sequencing on the collected nasal epithelium from long COVID (N=3) and post-COVID (N=3) individuals at baseline and after exposure to poly(I:C) and IFN-?