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Review
. 2024 Oct 16;12(10):2070.
doi: 10.3390/microorganisms12102070.

The Effect of Aloe vera on Skin and Its Commensals: Contribution of Acemannan in Curing Acne Caused by Propionibacterium acnes

Affiliations
Review

The Effect of Aloe vera on Skin and Its Commensals: Contribution of Acemannan in Curing Acne Caused by Propionibacterium acnes

Suraj Pal et al. Microorganisms. .

Abstract

Aloe vera is one of the most significant therapeutical plant species that belongs to the family Liliaceae. Aloe vera is composed of a high amount of water, with the remainder being dry matter. The dry matter contains a lot of bioactive compounds like carbohydrates, fats, and enzymes, with various therapeutic and antimicrobial properties. It can enhance the proliferation of cells and prevent cell damage by anti-oxidative properties (stimulating the secretion of superoxide dismutase and peroxidase). Human skin is colonized by microbes like fungi (Candida albicans), bacteria (Propionibacterium acnes, Staphylococcus aureus), and mites. These commensals are responsible for skin characteristics such as acidic pH, the pungent smell of sweat, etc. Human fetuses lack skin microbiota, and their skin is colonized after birth. Commensals present on the skin have a crucial role in training the human immune system against other pathogenic microbes. Propionibacterium acnes act as an opportunistic pathogen when the balance between the commensals is disturbed. We also emphasize the recent progress in identifying the aloe metabolite biosynthesis pathways and the associated enzyme machinery. The hyperproliferation of Propionibacterium acnes causes acne, and acemannan plays a significant role in its cure. Hence, we need to consider a new treatment approach based on the root cause of this dysbiosis.

Keywords: Aloe vera; Propionibacterium acnes; acemannan; antimicrobial; opportunistic pathogen; peroxidase; superoxide dismutase.

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Conflict of interest statement

Author Subhasish Saha was employed by Again Bio. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Dry matter composition. Aloe vera contains a large quantity of organic compounds including polysaccharides, enzymes, salicylic acid, tannins, fatty acids, vitamins, lectins, flavonoids, minerals (electrolytes), and proteins. Examples of these compounds are given in Table 1. Glucomannan and hemicellulose fibers are present in the aloe and play a crucial role in enhancing cellular proliferation. The anthracene derivative of quinone, also known as anthraquinones, is a laxative agent present in the aloe. Aloe-emodin and aloin are the two basic anthraquinones in aloe. Aloe-emodin is provided in powdered form as a laxative. The antioxidant (in vitro) properties of Aloe vera gel have been confirmed in some species of aloe including Aloe ferox, Aloe arborescens, Aloe greatheadii var Davyana, Aloe harlana, Aloe marlothii, Aloe melanacantha, and Aloe saponaria.
Figure 2
Figure 2
Mechanism of acne development by Propionibacterium acnes.
Figure 3
Figure 3
Anti-inflammatory mechanism of acemannan. (a) In peritoneal macrophage immune cells aloin inhibit the LPS-induced phosphorylation of ERK and JNK and inhibits secretion of Nitrogen oxide (NO) and cytokines of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and interleukin (IL)-1β. (b) Aloin can activate the Nrf2/HO-1 defense pathway, which can enhance the expression of HO-1and reduced inflammation in LPS-activated HUVECs by inhibiting NF-κB activity and the expression of iNOS, NO, COX2, and ILs. (c) Aloin significantly reduce HMGB1 release in LPS via SIRT1-mediated HMGB1 deacetylation. (d) Aloin drastically reduces LPS-stimulated inflammation pathway in cells by activation of ROS formation and hindering JAK1-STAT1/3. (e) Aloin mediates inhibition of inflammation associated with sepsis by affecting the release of growth factors in LPS induced HUVECs. (f) Aloin inhibiting necrosis factor, TNF-α and IL-6 in human endothelial cells.

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