Fig. 1.

Bacterial toxins andN-formyl peptides that modulate nociception.Mycobacterium ulcerans, a pathogen that leads to the Buruli ulcer, decreases pain sensation by secreting mycolactone which binds to angiotensin II receptor (AT2R) which leads to an increase of potassium to hyperpolarize nociceptors. Mycobacterium tuberculosis (Mtb), a pathogen that causes pulmonary tuberculosis (TB) activates nociceptors by secretion of sulfolipid-1 (SL-1). SL-1 increases calcium influx in these neurons to cause induce. Clostridium botulinum, Clostridium tetani secrete toxins such as botulinum neurotoxin (BoNT) and tetanus neurotoxin (TeNT) that block neurotransmission by cleaving SNARE proteins in neurons which prevents synaptic vesicles containing neurotransmitters from binding to synaptic cleft for release. Streptococcus pyogenes, a pathogen that causes necrotizing fasciitis, causes pain by release of the pore-forming peptide toxin streptolysin S (SLS), which leads to an influx of calcium. Staphylococcus aureus, a pathogen that leads to boils and painful rashes, activates neurons by release of 3 major classes of pore-forming toxins (PFTs) including α-haemolysin, phenol soluble modulin α3 (PSMα3) and γ-haemolysin AB. S. aureus and other gram-negative bacteria also secrete N-formyl peptides which can bind to formyl peptide receptors which can activate nociceptors to induce pain. Image created with BioRender.com.