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Figure 3. Residual inflammation is primed by prior obesity through partial maintenance of a proinflammatory profile in the heart. (A) Experimental schematic of the mouse study to assess immune-lipidome memory in naïve LV; (B) Fatty acids [arachidonic acid (AA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA)] in the LV of CON (10 months of lab chow), OBD (10 months of omega-6-enriched diet), and OBD-R (10 months of OBD diet + 4 months of CON diet) mice; (C) Schematic of AA, DHA, and EPA metabolic pathways; (D-F) Concentrations of (D) COX, (E) 12/15LOX, and (F) 5LOX products derived from AA in the LV; (G) Concentration of 12/15LOX products derived from DHA; (H) Concentration of 12/15LOX products derived from EPA. Quantification is reported as pg/50 mg LV tissue; detection limit ≈ 1 pg; (I) Stacked graphs showing average concentrations of prostaglandins (PGs) and hydroxyeicosatetraenoic acids (HETEs) in the LV; (J) Pie charts showing the distribution of AA, DHA, and EPA products. Percentages represent mean values for each identified lipid mediator; (K) Representative immunofluorescence images showing CCL2 (red) expression with cardiomyocyte area (WGA-yellow) in LV and CCL2 (red), F4/80 (green), and WGA (white) in adipocyte tissue. Nuclei are labeled with Hoechst (blue). Magnification, 40×. Scale bar, 50 μm; (L-S) Flow cytometry plots and quantification of CD45⁺, CD11b⁺, CCR2⁺, and F4/80⁺ populations in the LV. Comparisons were analyzed using one-way ANOVA with Tukey’s multiple comparisons test. *P < 0.05 vs. CON; #P < 0.05 vs. OBD. Data are presented as mean ± SEM; n = 4/group. LV: Left ventricle; CON: control diet; OBD: obesogenic diet; SEM: standard error of the mean; WGA: wheat germ agglutinin.