Suppression of Propionibacterium acnes-Induced Dermatitis by a Traditional Japanese Medicine, Jumihaidokuto, Modifying Macrophage Functions.

Kyoji Sekiguchi,Setsuya Aiba,Atsushi Kaneko,Seiichi Iizuka,Kenshi Yamasaki,Junichi Koseki,Yosuke Matsubara,Takashi Matsumoto,Kazuaki Tsuchiya,Sachiko Imamura,Junko Watanabe

doi:10.1155/2015/439258

Abstract

Purpose. Macrophages serve as sweepers of microbes and inflammation-derived wastes and regulators of inflammation. Some traditional Japanese medicines are reported to have adjuvant effects by modifying macrophages. Our aim was to characterize the actions of jumihaidokuto (JHT) for treatment of skin inflammations including acne vulgaris, in which Propionibacterium acnes has pathogenic roles. Methods. Dermatitis was induced in rat ears by intradermal injection of P. acnes. JHT or prednisolone (PDN) was given orally, and ear thickness and histology were evaluated. The effects of constituents and metabolites of JHT on monocytes were tested by cell-based assays using the human monocytic THP-1 cell. Results. JHT and PDN suppressed the ear thickness induced by P. acnes injection. Histological examinations revealed that JHT, but not PDN, promoted macrophage accumulation at 24 h after the injection. PDN suppressed the macrophage chemokine MCP-1 in the inflamed ears, while JHT did not affect it. The JHT constituents liquiritigenin and isoliquiritin increased expression of CD86 (type-1 macrophage marker) and CD192 (MCP-1 receptor) and enhanced phagocytosis by THP-1. Conclusions. JHT suppressed dermatitis, probably by enhancing type-1 macrophage functions, with an action different from PDN. JHT may be a beneficial drug in treatment of skin inflammation induced by P. acnes.

Highlights

Inflammation is the living body’s response to both exogenous and endogenous stimuli in order to exclude harmful stimuli and promote repair of injured tissue
Rats subjected to intradermal injection of P. acnes and given orally distilled water developed rapid ear swelling with cutaneous erythema
These results revealed that rats given JHT showed significantly more macrophage accumulation in the dermatitis induced by P. acnes than control rats

Summary

Introduction

Inflammation is the living body’s response to both exogenous and endogenous stimuli in order to exclude harmful stimuli and promote repair of injured tissue. The inflammatory spiral has recently been studied in order to understand the pattern recognition receptors and damage-associated molecular patterns involved in sterile inflammation [1, 2]. Neutrophils have high ability to kill foreign microbes but are remarkably short-lived and die at sites of inflammation. The targets of phagocytosis by macrophages are microbes and inflammation-derived wastes, including dead neutrophils. Type-2 macrophages directly and indirectly attenuate the inflammatory spiral, followed by promotion of wound healing [6]. Activation of macrophages is critical in sterile inflammation, the inflammatory response to cell and tissue damage, and the shift from acute to chronic inflammation

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