mRNA expression has been documented in fetal human intestine. Increased TLR4 expression has also been noted in
formula-fed and hypoxia-stressed rats. When LPS binds to
TLR4, abnormal TLR activation (perhaps via the influence of
PAF) occurs, and a series of chaperone and signal transduction
molecules are activated, which results in nuclear
factor-kB (NF-kB) translocation from cytoplasm to the nucleus,
where this important transcription factor activates the
gene expression of multiple proinflammatory cytokines.
Experiments have shown that mice with mutations in their
TLR4 gene are resistant to NEC.