Inflammation-Induced Viscosity Disrupts

Bacterial motility is a cornerstone of enteric infection dynamics, yet the biophysical impact of inflammation-induced mucus remodeling on flagellar propulsion remains underexplored. We present a multiscale modeling study of Salmonella enterica motility that integrates (i) a rotor– stator flagellar motor model linking torque generation to viscous load, (ii) low-Reynolds hydrodynamics in shear-dependent media (Carreau-type rheology), and (iii) active-matter metrics of collective behavior (run length, effective diffusivity, and clustering propensity). We show that inflammation-associated viscosity elevations impose a viscous torque that depresses motor rotation rate and propulsion efficiency, shortening run phases and suppressing coherent clustering. These effects emerge without altering chemotactic logic, indicating a primarily mechanical impediment to navigation. The framework reconciles clinical observations by suggesting phase-dependent outcomes: early, acute thickening impedes spread, whereas chronic remodeling may offset mechanical barriers via changes in turnover, structure, and nutrient/chemical landscapes. Although developed for peritrichous S. enterica, the load-matching principle generalizes to other flagellated enterics with species-specific quantitative thresholds. Our results motivate coupled experimental validation with mucus rheometry and single-cell tracking, and suggest testable strategies for therapeutic “rheological control” of colonization—either by preserving protective viscosity states or by targeting motor load–response coupling.