Acute inflammatory state during influenza infection and endothelial function

Chronic inflammatory stimulus seems to contribute to atherosclerotic process. Several studies have established a relationship between infective agents as Chlamydia pneumoniae, herpes virus and cytomegalovirus and atherosclerotic lesions. Aim of this study was to investigate the effects of influenza infective state on endothelial function of healthy young subjects, expressed as brachial flow-mediated vasodilation (FMV) and soluble form of intercellular adhesion molecule-1 (sICAM-1) and vascular cell adhesion molecule-1 (sVCAM-1). In 10 male subjects (mean age 35 ± 14 years) exhibiting influenza symptoms for 3 days, we determined total cholesterol, high-density lipoproteins (HDL), low-density lipoproteins (LDL), triglycerides, sVCAM-1, sICAM-1 and brachial FMV. All subjects had an antibody pattern characteristic of influenza A or B virus infection. After 3 months brachial FMV was significantly increased (8.6 ± 2.3% versus 11.5 ± 3.2%; p < 0.001), while HDL (46 ± 10 mg/dL versus 49 ± 9 mg/dL; p < 0.05), sICAM-1 and sVCAM-1 were reduced (respectively: 488 ± 105 ng/mL versus 340 ± 127 ng/mL; p < 0.001, 1710 ± 80 ng/mL versus 1216 ± 63 ng/mL; p < 0.001). Univariate analysis showed a positive correlation between changes in CRP and sICAM-1 levels (r = 0.95, p < 0.001), a negative one between changes in sICAM-1 and brachial FMV (r = −0.65, p < 0.05) and between CRP and brachial FMV (r = −0.64, p < 0.05). This small study suggested that inflammatory state determined by viral agents may transitorily alter endothelial function in healthy subjects.