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Macrophage Activation, Natural Products and Inflammatory Diseases

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Dear Colleagues,

Macrophages can be classified as M1 and M2 macrophages based on their polarization. M1 macrophages are classically activated by lipopolysaccharide and IFN-γ derived from tissue necrosis. After activation, M1 macrophages produce proinflammatory cytokines and phagocytize foreign microbes, thereby initiating an immune response. M2 macrophages, on the other hand, are alternatively activated by specific cytokines, such as IL-4, IL-10, or IL-13, decrease inflammation, and play crucial roles in wound healing, tissue repair, and tumor progression. In relation to atherosclerosis progression and regression, M1 macrophages predominate in progression and contribute to the inflammatory state, whereas M2 macrophages are enriched in many models of regression and appear to participate in inflammation resolution and plaque remodeling. Therefore, controlling the activity of macrophages can be an excellent strategy for controlling the inflammatory response provoked by infection, tissue repair, tumor progression, and atherosclerosis. Recently, there have been many reports of various natural products that can control macrophage activation. In this Special Issue, we will examine the action of natural products on macrophage activation and their potential as a treatment for inflammatory diseases or cancer progression. With this in mind, we are pleased to open this Special Issue for submissions.

Topics of interest include, but are not limited to:

Anti-inflammatory natural products with cytokine storm;
Action of natural products on acute inflammation;
Effect of natural products on chronic inflammatory diseases;
Future perspectives for anti-inflammatory natural products with macrophage activation;
Mechanisms of action of natural products;
Effect of natural products on arteriosclerosis;
Effect of natural products on tumor angiogenesis.

Prof. Dr. Wansu Park
Prof. Dr. Jai-eun Kim
Prof. Dr. Han-Sol Jeong
Guest Editors

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Keywords

natural product
macrophage
macrophage activation
anti-inflammation
cytokine
nitric oxide
cytosolic calcium
endoplasmic reticulum stress
cytokine storm
CHOP
pyroptosis

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13 pages, 9700 KiB

Open AccessArticle

Alleviative Effect of Geniposide on Lipopolysaccharide-Stimulated Macrophages via Calcium Pathway

by Hyun-Ju Kim and Wansu Park

Int. J. Mol. Sci. 2024, 25(3), 1728; https://doi.org/10.3390/ijms25031728 - 31 Jan 2024

Viewed by 655

Abstract

In this study, we investigated how geniposide (a bioactive ingredient of gardenia fruit) acts on lipopolysaccharide (LPS)-stimulated macrophages. Griess reagent assay, Fluo-4 calcium assay, dihydrorhodamine 123 assay, multiplex cytokine assay, quantitative RT-PCR, and flow cytometry assay were used for this study. Data showed that geniposide at concentrations of 10, 25, and 50 μM reduced significantly the levels of nitric oxide, intracellular Ca²⁺, and hydrogen peroxide in LPS-activated RAW 264.7. Multiplex cytokine assay showed that geniposide at concentrations of 10, 25, and 50 μM meaningfully suppressed levels of IL-6, G-CSF, MCP-1, and MIP-1α in RAW 264.7 provoked by LPS; additionally, geniposide at concentrations of 25 and 50 μM meaningfully suppressed the levels of TNF-α, IP-10, GM-CSF, and MIP-1β. Flow cytometry assay showed that geniposide reduces significantly the level of activated P38 MAPK in RAW 264.7 provoked by LPS. Geniposide meaningfully suppressed LPS-induced transcription of inflammatory target genes, such as Chop, Jak2, Fas, c-Jun, c-Fos, Stat3, Nos2, Ptgs2, Gadd34, Asc, Xbp1, Nlrp3, and Par-2. Taken together, geniposide exerts alleviative effects in LPS-stimulated macrophages via the calcium pathway. Full article

(This article belongs to the Special Issue Macrophage Activation, Natural Products and Inflammatory Diseases)

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9 pages, 5771 KiB

Open AccessArticle

Citri Reticulatae Pericarpium Limits TLR-4-Triggered Inflammatory Response in Raw264.7 Macrophages by Activating RasGRP3

by Ji Hye Lee, Yon-Suk Kim and Kang Hyun Leem

Int. J. Mol. Sci. 2023, 24(18), 13777; https://doi.org/10.3390/ijms241813777 - 07 Sep 2023

Cited by 1 | Viewed by 792

Abstract

Inflammation is an important immune response to pathogen invasion, but excessive inflammation leads to tissue injury and even cytokine storm. Therefore, proper response is needed depending on the intensity of the infection. Ras guanine nucleotide releasing protein 3 (RasGRP3) is a regulator of the TLR-mediated response. In low-intensity inflammation, it negatively regulates production of pro-inflammatory cytokines, especially IL-6. Citri Reticulatae Pericarpium, the peel of Citrus reticulata Blanco, is a major medicinal herb in Korean medicine. The present study aims to investigate whether the Citri Reticulatae Pericarpium extract (CRE) has immunomodulatory activity using the Raw264.7 macrophage. Also, we investigated the effect of CRE on RasGRP3 expression. In the present study, CRE reduced IL-6 production in the low-LPS environment (1 ng/mL) and did not in the high-LPS environment (100 ng/mL). The suppression of IL-6 production in the low-LPS environment (1 ng/mL) was abolished after the pretreatment of RasGRP3 siRNA. The reduced RasGRP3 protein content by 100 ng/mL LPS treatment was increased by CRE treatment. Additionally, nobiletin, a major component of CRE showed a suppressive effect on IL-6 production in the low-LPS environment (1 ng/mL). The present results suggest that CRE alleviates inflammatory response via activating RasGRP3 expression in low-intensity inflammation. Full article

(This article belongs to the Special Issue Macrophage Activation, Natural Products and Inflammatory Diseases)

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