Figure 3. Atherosclerotic vascular disease parameters.

(A) The total aortic plaque area was measured and an increase in plaque area (mm²) was found for polymicrobial-infected ApoE^null mice when compared to sham-infected control mice (P<0.05). (B) Intimal/medial thickness ratios were determined and an increase was observed in the polymicrobial-infected mice compared to sham-infected mice. Polymicrobial infection-induced macrophage infiltration in ApoE^null mice. 4 µm thick paraffin embedded sections of the aortic arch were cut and stained with H&E; (C) Number of macrophage per total adventitial area. (D) Number of macrophage per total intimal area. Control indicates sham-infected ApoE^null mice and Pg+Td+Tf indicate polymicrobial-infected mice. An increase in macrophages was seen in both the adventitial and intimal layers in the polymicrobial-infected mice when compared to the sham-infected mice. Histologic evaluation of 4 µm thick paraffin embedded aortic arch sections stained using H? plaque area is flanked with black arrows, macrophage infiltration is indicated using white arrow with open head and cholesterol crystals are indicated using white arrows with filled heads. (E) Sham-infected control mice tissue (Magnification 40×); (F) Pg, Td, and Tf infection mice tissue (Magnification 40×) containing larger plaque area, increased macrophage infiltration and increased presence of cholesterol crystals, suggesting polymicrobial infection-induced aortic plaque and aortic wall thickness in ApoE^null mice.