LAP-TLR2 Axis Drives Inflammatory Pathology during Listeria monocytogenes Gastroenteritis

A high-dose Listeria monocytogenes infection (~1x10^10 CFU/mouse) triggers early, epithelial-eroding gastroenteritis with profound neutrophil infiltration in mice, linked to LAP-driven TLR2 signaling.

• Why it matters: The enteric phase precedes invasive listeriosis, but how bacterial virulence programs coordinate with host inflammation in the gut is not well defined.
• What they did: The study used a mouse gastroenteritis model, mRNA-seq, HEK-Dual hTLR2 (NF-kB) reporter cells, and TLR2 knockout mice to test whether LAP—rather than internalin A or listeriolysin O—activates the TLR2-MyD88 pathway and TNFalpha.
• The result: LAP engages TLR2 to activate NF-kB and compromises the epithelial barrier; severity tracks myeloid hyperactivation and ion channel dysregulation, and MLCK-dependent tight junction opening is required for paracellular neutrophil migration.

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