Congratulations to Dr Julie Worrell on her recently published research in Nature Communications. Dr Worrell was the lead/corresponding author on the publication titled ‘Lung structural cells are altered by influenza virus leading to rapid immune protection following re-challenge’.
Explaining this important research, Dr Worrell says, ‘‘Our findings suggest that lung structural cells function as much more than a passive scaffold, instead playing an active role in antiviral defence, and are capable of ‘remembering’ past infections. Understanding how these cells store and use this memory could lead to vaccines and therapies that provide stronger, longer-lasting protection against respiratory viruses. By identifying key molecules that control this response, we hope to harness this tissue memory to boost immunity, potentially opening new strategies for preventing and treating infections like Influenza, RSV, and COVID-19.’’
As stated by Dr Worrell and Prof Megan Macleod in a blog post regarding this research, ‘the expanding field of structural immunology, while previously neglected, may help us to identify new allies in the fight against respiratory pathogens. We are only beginning to explore these possibilities’.
Abstract
Lung structural cells form barriers against pathogens and trigger immune responses following infections. This leads to the recruitment of innate and adaptive immune cells some of which remain within the lung and contribute to enhanced pathogen control following subsequent infections. There is growing evidence that structural cells also display long-term changes following infection. Here we investigate long-term changes to mouse lung epithelial cells, fibroblasts, and endothelial cells following influenza virus infection finding that all three cell types maintain an imprint of the infection, particularly in genes linked to communication with T cells. MHCI and MHCII proteins continue to be expressed at higher levels in both differentiated epithelial cells and progenitor populations and several differentially expressed genes are downstream of the transcription factor, SpiB, a known orchestrator of antigen presentation. Lung epithelial cells from influenza-infected mice display functional changes, more rapidly controlling influenza virus than cells from naïve animals. This rapid anti-viral response and increased expression of molecules required to communicate with T cells demonstrates sustained and enhanced functions following infection. These data suggest lung structural cells display characteristics of immune memory which could affect outcomes that are protective in the context of infection or pathogenic in chronic inflammatory disorders.
Read the full paper here.