What question did this study set out to answer?

This research aims to investigate how RSV affects macrophage immune functions through SIGLEC1 modulation.

April 22, 2026Open Access

Respiratory syncytial virus–induced SIGLEC1 upregulation inhibits macrophage autophagy and facilitates inflammatory mediator secretion

FLFuhuang LaiFujian Medical University ALAirong LiaoFujian Medical University KXKang XiaFujian Medical University

Puntos clave

This research aims to investigate how RSV affects macrophage immune functions through SIGLEC1 modulation.
Infection of THP-1-derived macrophages with RSV monitored using fluorescence microscopy.
Assessment of SIGLEC1 expression and macrophage viability through RT-qPCR, western blot, and CCK-8 assays.
Evaluation of autophagy levels and inflammatory responses by various biochemical and imaging techniques.
RSV infection led to significant macrophage activity repression and increased SIGLEC1 expression.
The upregulation of SIGLEC1 inhibited autophagy, with decreased levels of ATG5 and LC3II.
Macrophages were polarized towards the M1 phenotype, resulting in elevated secretion of proinflammatory cytokines.

Resumen

Background Respiratory syncytial virus (RSV) is a leading culprit behind respiratory infections in infants. As a cornerstone of the immune defence, macrophages are instrumental in warding off invading pathogens. This study examines the molecular pathways through which RSV modulates the immune functions of macrophages during infection. Methods THP-1–derived macrophages were infected with RSV, and the infection was monitored using fluorescence microscopy. The viability of infected macrophages was measured using CCK-8, and SIGLEC1 expression was analysed by RT-qPCR and western blot (WB). Gene set enrichment analysis was performed to identify pathways associated with SIGLEC1 enrichment. SIGLEC1-knockdown macrophages were developed, and autophagy levels in these cells following RSV infection were examined using WB, immunofluorescence and monodansylcadaverine staining. The influence of RSV infection on macrophage phenotype and inflammatory responses was assessed through morphological observation, flow cytometry, ELISA and nitric oxide synthase expression analysis. Results Following RSV infection, macrophage activity was significantly repressed, and SIGLEC1 expression was markedly upregulated. This upregulation of SIGLEC1 effectively suppressed the autophagy process in macrophages, as indicated by decreased levels of ATG5 and LC3II, and reduced autophagosome formation. RSV infection also drove macrophages towards the M1 phenotype, which was accompanied by increased secretion of proinflammatory cytokines. Importantly, these effects were reversible through SIGLEC1 knockdown or treatment with an autophagy activator, which restored autophagy levels and curbed the release of inflammatory mediators. Conclusion By exposing how RSV exploits SIGLEC1 to inhibit macrophage autophagy, reinforce M1 polarisation and increase cytokine secretion, this study lays vital groundwork for new treatments targeting this viral scourge.

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