Abstract

Mentha piperita L. (peppermint) possesses antimicrobial properties, but little is known of its ability to modulate macrophages. Macrophages are essential in bacterial infection control due to their antimicrobial functions and ability to link the innate and adaptive immune responses. We evaluated the effects of the peppermint leaf hydroalcoholic extract (LHAE) on cultured murine peritoneal macrophages stimulated or not with lipopolysaccharide (LPS) in vitro. Vehicle-treated cells were used as controls. The constituents of the extract were also identified. Epicatechin was the major compound detected in the LHAE. LPS-induced macrophage death was reversed by incubation with LHAE (1–30 μg/ml). Higher concentrations of the extract (≥100 μg/ml) decreased macrophage viability (49–57%) in the absence of LPS. LHAE (1–300 μg/ml) attenuated H2O2 (34.6–53.4%) but not nitric oxide production by these cells. At similar concentrations, the extract increased the activity of superoxide dismutase (15.3–63.5-fold) and glutathione peroxidase (34.4–73.6-fold) in LPS-treated macrophages. Only LPS-unstimulated macrophages presented enhanced phagocytosis (3.6–6.6-fold increase) when incubated with LHAE (3–30 μg/ml). Overall, the LHAE obtained from peppermint modulates macrophage-mediated inflammatory responses, by stimulating the antioxidant pathway in these cells. These effects may be beneficial when the excessive activation of macrophages contributes to tissue damage during infectious disease.

Highlights

  • Macrophages are on the first line of the host’s immune response to bacterial infection

  • Peppermint leaf hydroalcoholic extract (LHAE) effects were evaluated on macrophage viability stimulated or not with LPS

  • We investigated the effects of a peppermint LHAE on cultured macrophages stimulated or not with LPS from K. pneumoniae

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Summary

Introduction

Macrophages are on the first line of the host’s immune response to bacterial infection. Gram-negative bacterial strains are major pathogens causatives of severe infectious diseases in humans, associated with high mortality rates [4, 5]. This is due to their ability to become resistant to the available antimicrobials [4] and depends on an effective macrophage response to these pathogens [6]. The production of oxidant species by macrophages is a hallmark of the inflammatory response to infection (see for Journal of Immunology Research review [7, 8]). Alongside an excessive nitric oxide (NO) production, increased levels of prooxidant species may lead to damage and poor perfusion of vital organs of the host, contributing to multiple organ failure; to counteract this response, antioxidant pathways are activated [10]

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