Abstract
BackgroundMacrophages are crucial players in a variety of inflammatory responses to environmental cues. However, it has been widely reported that macrophages cause chronic inflammation and are involved in a variety of diseases, such as obesity, diabetes, metabolic syndrome, and cancer. In this study, we report the suppressive effect of 5-aminolevulinic acid (ALA), via the HO-1-related system, on the immune response of the LPS-stimulated mouse macrophage cell line RAW264.7.ResultsRAW264.7 cells were treated with LPS with or without ALA, and proinflammatory mediator expression levels and phagocytic ability were assessed. ALA treatment resulted in the attenuation of iNOS and NO expression and the downregulation of proinflammatory cytokines (TNF-α, cyclooxygenase2, IL-1β, IL-6). In addition, ALA treatment did not affect the phagocytic ability of macrophages. To our knowledge, this study is the first to investigate the effect of ALA on macrophage function. Our findings suggest that ALA may have high potential as a novel anti-inflammatory agent.ConclusionsIn the present study, we showed that exogenous addition of ALA induces HO-1 and leads to the downregulation of NO and some proinflammatory cytokines. These findings support ALA as a promising anti-inflammatory agent.
Highlights
Macrophages are crucial players in a variety of inflammatory responses to environmental cues
These results suggest that aminolevulinic acid (ALA) addition induces Heme oxygenase-1 (HO-1) protein expression without noticeable cell damage in RAW264.7 cells
INOS and Nitric oxide (NO) expression analysis of RAW264.7 macrophages under LPS stimulation with ALA Since we evaluated the effect of ALA alone on HO-1, we investigated the effect of ALA on the activity of the macrophage cell RAW264.7
Summary
Macrophages are crucial players in a variety of inflammatory responses to environmental cues. It has been widely reported that macrophages cause chronic inflammation and are involved in a variety of diseases, such as obesity, diabetes, metabolic syndrome, and cancer. We report the suppressive effect of 5-aminolevulinic acid (ALA), via the HO-1-related system, on the immune response of the LPS-stimulated mouse macrophage cell line RAW264.7. A number of recent investigations have indicated the important relationship between the particular steps of colorectal cancer development and inflammation due to obesity, which is mediated by proinflammatory cytokines (e.g., interleukin-6 (IL-6)) and tumor necrosis factor-α (TNF-α) secreted by macrophages [2, 3]. To avoid lifestyle-related diseases caused by macrophages, it is important to prevent abnormal activation and to keep macrophages within their proper range of activity. Since LPS is widely used in studies of inflammation and chronic inflammation can be modeled by administration of LPS in vivo [4, 5], we used LPS to study inflammation in an in vitro model
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