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Residual inflammation in cardiovascular organs is thought to be one of the catalysts for the increased risk of cardiovascular complications seen following pneumonia. To test this hypothesis, we investigated changes in plaque characteristics and inflammatory features in ApoE-/- mouse aorta and heart following pneumonia. Male ApoE-/- mice were fed a high fat diet for 8 weeks before intranasal inoculation with either Streptococcus pneumoniae serotype 4 (test group) or phosphate buffered saline (control group). Mice were sacrificed at 2-, 7- and 28-days post-challenge. Changes in plaque burden and characteristics in aortic root and thoracic aorta were characterized by Oil red O and Trichrome stains. Inflammatory changes were investigated by FDG-PET imaging and immunofluorescence staining. We found TIGR4-infected mice present with increased plaque presence in the aortic root and thoracic aorta at 2- and 28-days post-inoculation, respectively. Aortic wall remodelling was also more pronounced in mice challenged with pneumococci at 28 days post-inoculation. Aortic root plaques of infected mice had reduced collagen and smooth muscle cells, consistent with an unstable plaque phenotype. Pneumonia alters plaque burden, plaque characteristics, and aortic wall remodelling in ApoE-/- mice. These effects caused by Streptococcus pneumoniae TIGR4, may contribute to the increased risk of cardiovascular complications seen in survivors of this infection., (© 2022. The Author(s).)

Atherosclerosis is now considered a chronic maladaptive inflammatory disease. The hallmark feature in both human and murine disease is atherosclerotic plaques. Macrophages and various T-cell lineages play a crucial role in atherosclerotic plaque establishment and disease progression. Humans and mice share many of the same processes that occur within atherogenesis. The various similarities enable considerable insight into disease mechanisms and those which contribute to cardiovascular complications. The apolipoprotein E-null and low-density lipoprotein receptor-null mice have served as the foundation for further immunological pathway manipulation to identify pro- and antiatherogenic pathways in attempt to reveal more novel therapeutic targets. In this review, we provide a translational perspective and discuss the roles of macrophages and various T-cell lineages in contrasting proatherosclerotic and atheroprotective settings.