Lipopolysaccharide-Induced Cytokine and Chemokine Expression in Human Carotid Lesions

Abstract

The release of cytokines and chemokines from activated immune-competent cells plays a crucial role in determining the pathology of the atherogenic progress. We investigated the effect of bacterial lipopolysaccharide (LPS) on cytokine/chemokine expression in carotid lesions and normal renal arteries. The lesions or renal arteries were incubated for 6 h at 37°C in serum-free media treated with or without LPS. After LPS treatment, increased protein levels of IL-1β, IL-6, IL-8, IL-10, TNF-α and MCP-1 were observed in the culture medium from the lesions measured with cytometric bead array. We were able to detect the induction of IL-1β, IL-6, IL-8, IL-10, TNF-α and MCP-1 mRNA in the lesions after stimulation with LPS using real-time PCR. In renal arteries, LPS also induces mRNA expression of all chemokines and cytokines investigated with the exception of IL-6. However, LPS induces significantly higher levels of TNF-α, IL-1β and IL-10 mRNA in lesions compared to renal arteries. The results suggest that infectious agents are capable of enhancing the production of cytokines/chemokines in an already ongoing inflammatory process such as in atherosclerosis, and that low levels of circulating LPS may affect the levels of pro-inflammatory cytokines much more in atherosclerotic vessels than in normal vessels and may contribute to the development of the atherosclerotic lesion.

Expression of IL-1β, IL-1 Receptor Type I and IL-1 Receptor Antagonist in Human Aortic Smooth Muscle Cells: Effects of all-<i>trans</i>-Retinoic Acid

“…Gene expression was normalized to β-actin gene expression [19]. Each sample was analyzed in duplicate under the following conditions: 2 min at 50°C, 10 min at 95°C, 0.15 min at 95°C and 1 min at 60°C.…”

Sitagliptin attenuates inflammatory responses in lipopolysaccharide-stimulated cardiomyocytes via nuclear factor-κB pathway inhibition

“…It was shown that LPS participates in the inflammatory response by resulting in enhanced expression of proinflammatory cytokines such as TNF-α and causes dysfunction in the cardiovascular system (22). Under septic conditions, excessive LPS enhances the expression of proinflammatory cytokines and chemokine cascades via the activation of TLR-4.…”

Cytokine secretion from monocytes persists differentially after activator removal—One mechanism of long‐term biological response to implants

“…These infections can be cured only by an aggressive treatment of the infection, or even removal of the implant 7, 8. More recently, the effects of less‐frequent or low‐grade inflammation has been linked to implant‐associated disease and systemic disease states 9–16. For example, chronic loss of bone support around orthopedic implants may result from a low grade, intermittent inflammatory activation of monocytes near the implant 17, 18.…”