Abstract

The SCN9A gene encodes the voltage-gated sodium channel Nav1.7, a key determinant of nociceptive signal initiation and pain perception. Pathogenic variants in SCN9A cause either extreme pain syndromes or congenital insensitivity to pain, underscoring the central role of sodium channel biology in pain physiology. Infection-related pain represents a major clinical burden and is often prolonged or exacerbated by antibiotic resistance. Beyond neuronal signaling, sodium ions and osmotic balance exert important effects on immune function, bacterial physiology and antimicrobial activity. This hypothesis paper proposes that sodium homeostasis constitutes a shared biological axis linking pain perception, host defense and bacterial adaptability. We further hypothesize that combining physiological saline with the metal chelator Ethylene Diamine Tetra Acetic Acid (EDTA) and conventional antibiotics may attenuate bacterial resistance by disrupting osmoregulatory and ion-dependent defense mechanisms, thereby indirectly improving infection-associated pain outcomes. This framework integrates neurogenetics with microbial physiology and outlines experimentally testable predictions.

Keywords:SCN9A; Nav1.7; Pain signaling; Sodium homeostasis; Osmolality; Antibiotic resistance; EDTA