Alison J Carey

Combining human cord blood monocytes with a neonatal mouse influenza model, this study found that neonatal monocytes sustain higher TLR2 expression after LTA or IAV stimulation, while TLR2 gene deletion, anti-TLR2 antibody blockade, or myeloid-specific TLR2 deletion improved survival of IAV-infected neonatal mice (for example, 61% versus 25% survival for TLR2−/− versus wild-type neonates, and 46% versus 7% with anti-TLR2 antibody), accompanied by reduced neutrophils at 6 days post-infection, lower histopathology scores in myeloid conditional knockouts, and no further rise in IL-6, TNF-α, MCP-1, CXCL1, and CXCL2 from 3 to 6 days post-infection, suggesting that myeloid TLR2 signaling exacerbates neonatal susceptibility to respiratory viral infection by amplifying pulmonary inflammation.

Combining human cord blood monocytes with a neonatal mouse influenza model, this study found that neonatal monocytes sustain higher TLR2 expression after LTA or IAV stimulation, while TLR2 gene deletion, anti-TLR2 antibody blockade, or myeloid-specific TLR2 deletion improved survival of IAV-infected neonatal mice (for example, 61% versus 25% survival for TLR2−/− versus wild-type neonates, and 46% versus 7% with anti-TLR2 antibody), accompanied by reduced neutrophils at 6 days post-infection, lower histopathology scores in myeloid conditional knockouts, and no further rise in IL-6, TNF-α, MCP-1, CXCL1, and CXCL2 from 3 to 6 days post-infection, suggesting that myeloid TLR2 signaling exacerbates neonatal susceptibility to respiratory viral infection by amplifying pulmonary inflammation.