Medical Potential of Insect Symbionts

Abstract

Insect symbionts and their metabolites are complex and diverse and are gradually becoming an important source of new medical materials. Some culturable symbionts from insects produce a variety of active compounds with medical potential. Among them, fatty acids, antibacterial peptides, polyene macrolides, alkaloids, and roseoflavin can inhibit the growth of human pathogenic bacteria and fungi; lipases, yeast killer toxins, reactive oxygen species, pyridines, polyethers, macrotetrolide nactins, and macrolides can kill human parasites; and peptides and polyketides can inhibit human tumors. However, due to difficulty in the culture of symbionts in vitro, difficulty in targeting bacteria to specific sites in the human body, the limited capability of symbionts to produce active metabolites in vitro, inconsistent clinical research results, adverse reactions on humans, and the development of antibiotic resistance, the application of insect symbionts and their metabolites in the medical field remains in its infancy. This paper summarizes the medical potential of insect symbionts and their metabolites and analyzes the status quo and existing problems with their medical application. Possible solutions to these problems are also proposed, with the aim of hastening the utilization of insect symbionts and their metabolites in the medical field.

Keywords: antibiotic; antiparasitic activity; antitumor activity; insect symbiont; medical application; secondary metabolite.

Figure 1

Effects of insect symbiont metabolites on pathogenic bacteria and fungi. (A) Effects of short-chain fatty acids on pathogenic bacteria; (B) Effects of long-chain fatty acids on pathogenic bacteria; (C) Effects of antibacterial peptides on pathogenic bacteria; (D) Effects of polyene macrolides on pathogenic fungi; (E) Effects of alkaloids on pathogenic bacteria; (F) Effects of roseoflavin on pathogenic bacteria. Arrows depict activation in interactions.

Figure 2

A selection of antibacterial compounds isolated from insect symbionts. (A) Conocandin B; (B) Conocandin C; (C) Lenzimycin A; (D) Lenzimycin B; (E) Nicrophorusamide A; (F) Candicidin D; (G) Selvamicin; (H) Coprisidin B; (I) Roseoflavin.

Figure 3

Inhibition of the growth of the malaria parasite (A) and Leishmania donovani (B) by insect symbiont metabolites. Red arrows depict activation, while red bars represent suppression in molecular interactions. Thicker lines represent high flow rates. Dashed lines divide the cells into the normal half and the half in which the metabolites of insect symbionts exert antiparasitic effects.

Figure 4

A selection of antiparasitic compounds isolated from insect symbionts. (A) Mer-A2026B and piericidin-A₁; (B) Nigericin; (C) Dinactin; (D) Cyphomycin; (E) Caniferolide C and GT-35.

Figure 5

Effects of insect symbiont metabolites on tumor cells. Arrows depict activation, while bars represent suppression in molecular interactions. Abbreviations: Akt/mTOR/p70S6K—protein kinase B/mammalian target of rapamycin/p70 ribosomal protein S6 kinase; bad, bax, fasl, and p53—pro-apoptotic genes; bcl-2 and bcl-xL—anti-apoptotic genes; Cyclin B1, cdc2, and D3—positive regulators of cell cycle progression; Cyclin p21—a negative regulator of cell cycle progression; HIF1α—the hypoxia-inducible factor 1α; IFN-γ—interferon gamma; IL-9—immunomodulatory factor interleukin-9; MMP-2/MMP-9—matrix metalloproteinase MMP-2/MMP-9; PI3K/Akt—phosphatidylinositol 3-kinase/protein kinase B; p27 Kip1—an inhibitor of the cell cycle; TNF-α—tumor necrosis factor alpha; VEGFR—vascular endothelial growth factor receptor.

Figure 6

A selection of antitumor compounds isolated from insect symbionts. (A) Enniatin S; (B) Culicinin D; (C) Actinomycin D; (D) A new spectinabilin derivative; (E) Secalonic acid D; (F) Aspertaichunol A; (G) Bostrycin; (H) WBI-1001.