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. 2020 Apr 22;9(4):1190. doi: 10.3390/jcm9041190

Figure 2.

Figure 2

Pruriceptor neurons recognize skin pathogens and their molecular ligands by various mechanisms to facilitate itch. LPS, a key cell wall component of Gram-negative bacteria attaches to neuronal TLR4 and primes TRPV1 ion channel or opens the TRPA1 ion channel. S. aureus triggers itch with bacterial N-formyl peptides that bind to FPR1 or via α-hemolysin, which couples with ADAM10. C. albicans stimulates pruriceptors with its cell wall component zymosan. Viral double-strand RNA and single-strand RNA bind to TLR3 and TLR7, respectively, which are believed to sensitize the TRPA1 ion channel. ADAM10: a disintegrin and metalloproteinase domain-containing protein 10; FPR1: formyl peptide receptor 1; LPS: lipopolysaccharide; RNA: ribonucleic acid; TLR: Toll-like receptor; TRPA1: transient receptor potential ankyrin 1; TRPV1: transient receptor potential vanilloid 1.