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Research validates inflammaging theory

January 20 2017. Inflammaging, defined as chronic, systemic low-grade inflammation that occurs with aging in the absence of overt infection, has been hypothesized as a mechanism of age-associated disease and premature mortality. A cause of inflammaging has been attributed to lifetime exposure to a variety of antigens via the intestine.

In an article published on January 3, 2017 in Scientific Reports, Korean researchers report the finding in mice of an age-related decrease in supportive pericytes that surround the intestinal blood vessels’ endothelial cells, which increases vascular leakage. This phenomenon was ascribed to upregulation of angiopoetin-2 in the microvascular endothelial cells due to the inflammatory cytokine tumor necrosis factor-alpha (TNF-a) that originates from a type of macrophage (white blood cells that consume foreign antigens and other undesirable material).

“A hallmark of age-associated chronic inflammation would be macrophage infiltration,” the authors explain. “In intestine, the epithelial lining separates internal organs from the enteric environment loaded with various foreign substances including microbiota and its metabolic products as well as nutrients and wastes.”

“Antigenic burdens encountered in intestine throughout life create the condition of chronic stage of inflammation, which accumulates M2-like macrophages expressing TNF-α,” they write. “The TNF-α induces vascular leakage to facilitate recruitment of immune cells into intestine under the chronic inflammatory setting.”

"This study is significant as we have newly identified the mechanisms of aging associated with inflammation increase and opened possibilities of applied researches on aging delay through inflammation control as well as anti-aging,” commented lead researcher Sang Chul Park. “We will conduct follow-up studies to find ways to extend human healthy life by controlling inflammatory cells and vascular leakage to delay aging."

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