An insight of oil protection theory: Survival, structural and metabolic adaptation of Salmonella enterica Enteritidis Phage Type 30 in three triglycerides

Oil protection theory posits that oil enhances microbial survival and heat resistance in low-moisture foods, yet the role of triglyceride composition remains poorly defined. This study investigates how Salmonella enterica Enteritidis PT 30 adapts during desiccation in peanut oil (mixed triglycerides, aw,25 degrees C = 0.30) and two representative components, namely, trilinolein and glyceryl trioleate. The lipid-specific structural and metabolic adaptations were analyzed through confocal microscopy and transcriptomics. S. Enteritidis exhibited the lowest persistence (3.43-log reduction over 180 days) and weakest heat resistance (2.5 h at 80 degrees C to achieve 3.5-log reduction) in peanut oil. The survival of S. Enteritidis in triglycerides could be correlated with its metabolic dormancy via suppression of ribosomal and oxidative phosphorylation pathways. Trilinolein enhanced S. Enteritidis' heat resistance (30 h at 80 degrees C for 3.5-log reduction) and moderate storage mortality (1.64-log reduction at 180 d), driven by stress hyperactivity. Glyceryl trioleate balanced heat tolerance (8 h) with optimal storage survival (1.19-log reduction), mediated by partial metabolic suppression. Peanut oil preserved S. Enteritidis transient motility in water-rich microenvironments, while pure triglycerides formed compact, dehydrated aggregates. Transcriptomics identified divergent strategies. Peanut oil induced dormancy at the expense of stress resilience, whereas homogeneous lipids imposed distinct constraints; that is, trilinolein amplified oxidative stress, and glyceryl trioleate intensified desiccation. These findings refine oil protection theory, demonstrating that lipid heterogeneity-not just low water activity-shapes microbial outcomes. The mixed components of peanut oil buffer stress but limit protective efficacy, while its purified constituents reveal how specific triglycerides modulate survival. This mechanistic understanding advances theoretical models of pathogen persistence in oily matrices and guides targeted strategies to mitigate risks in low-moisture oil-rich food systems.