Ginseng alleviates microbial infections of the respiratory tract: a review

J Ginseng Res. 2020 Mar;44(2):194-204. doi: 10.1016/j.jgr.2019.12.001. Epub 2019 Dec 12.

Abstract

The detrimental impact of air pollution as a result of frequent exposure to fine particles posed a global public health risk mainly to the pulmonary disorders in pediatric and geriatric population. Here, we reviewed the current literature regarding the role of ginseng and/or its components as antimicrobials, especially against pathogens that cause respiratory infections in animal and in vitro models. Some of the possible mechanisms for ginseng-mediated viral inhibition suggested are improvements in systemic and mucosa-specific antibody responses, serum hemagglutinin inhibition, lymphocyte proliferation, cell survival rate, and viral clearance in the lungs. In addition, ginseng reduces the expression levels of proinflammatory cytokines (IFN-γ, TNF-α, IL-2, IL-4, IL-5, IL-6, IL-8) and chemokines produced by airway epithelial cells and macrophages, thus preventing weight loss. In case of bacterial infections, ginseng acts by alleviating inflammatory cytokine production, increasing survival rates, and activating phagocytes and natural killer cells. In addition, ginseng inhibits biofilm formation and induces the dispersion and dissolution of mature biofilms. Most clinical trials revealed that ginseng, at various dosages, is a safe and effective method of seasonal prophylaxis, relieving the symptoms and reducing the risk and duration of colds and flu. Taken together, these findings support the efficacy of ginseng as a therapeutic and prophylactic agent for respiratory infections.

Keywords: ARI, acute respiratory illness; Bacteria; COPD, chronic obstructive pulmonary disease; Clinical trials; GSLS, ginseng stem–leaf saponins; Ginseng; HRV, human rhinovirus; IFN, interferon; IL, interleukin; IgA, immunoglobulin A; PD, protopanaxadiol; PT, protopanaxatriol; ROS, reactive oxygen species; RSV, respiratory syncytial virus; RTIs, respiratory tract infections; Respiratory tract infections; TNF-α, tumor necrosis factor-alpha; Virus.

Publication types

  • Review