A healthy smile could reduce your likelihood of having a heart attack. Clinical and epidemiological studies indicate that common chronic infections may contribute to up to 40% of newly developed atherosclerotic cases. It has been proposed this phenomenon is linked to common mechanisms of Toll-Like Receptor (TLR)-mediated signaling triggered by a variety of pathogens, one being Porphyromonas gingivalis, an inducer of oral bone destruction that manifests as periodontal disease in more than 100 million people in the US alone. The observation of dysregulated innate immune signaling within P. gingivalis-triggered atherosclerotic lesions sparked interest in the association between oral infection and induction of innate immune cascades in atherosclerosis progression. In the study conducted by Chie Hayashi and coworkers from Boston University School of Medicine, atherosclerosis prone apolipoprotein-E null (ApoE-/-) and TLR4-deficient (ApoE-/-TLR4-/-) mice were orally infected with the periodontal pathogen P. gingivalis showing that ApoE-/-TLR4-/- mice were markedly more susceptible to atherosclerosis after oral infection. Immunohistochemical analysis of lesions from ApoE-/-TLR4-/- mice revealed an increased inflammatory cell infiltrate composed primarily of macrophages and IL-17 effector T cells (Th17), a subset linked with chronic inflammation. Furthermore, enhanced atherosclerosis in TLR4-deficient mice was associated with impaired development of Th1 immunity and regulatory T cell infiltration (evaluated using Enzo’s anti-mouse FoxP3 antibody). In conclusion their findings again point to a role for pathogen-specific TLR signaling in chronic inflammation and atherosclerosis and demonstrate an atheroprotective role for TLR4 in response to infection with the oral pathogen P. gingivalis.
Enzo Life Sciences offers a comprehensive range of antibodies that are tested and validated in immunohistochemical/immunofluorescent techniques, some of which are given below: