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HOME > What's LPS > Skincare and LPS / Atopic dermatitis and LPS

Skincare and LPS

(6) Atopic dermatitis and LPS

LPS is effective in improving atopic dermatitis (AD) (*1, 2).

People with genetic abnormalities in filaggrin, a barrier function protein, are susceptible to AD (*3). When the barrier function is incomplete, it is easier for antigens to enter the body from the outside and induce allergies. When epidermal keratinocytes are stimulated by LPS, the expression of filaggrin is enhanced (*4), which suggests an association with the AD improvement effect of LPS. In addition, when filaggrin is metabolized to amino acids, it works as a natural moisturizing factor (NMF) to enhance moisture.

LPS induces filaggrin, a barrier function protein, in the epidermis

In AD, skin commensal bacteria which are not normally harmful, such as Staphylococcus aureus, propagate abnormally, and such condition aggravates the symptoms (*5). It has been reported that antibiotic administration is effective in improving AD. When keratinocytes are stimulated by LPS, β-defensins (endogenous antimicrobials) are induced (*6). In other words, by using LPS, without drugs, endogenous antimicrobials are induced, and propagation of skin commensal bacteria can be controlled to some extent. This endogenous antimicrobial induction is thought to be one of the reasons for the LPS-induced improvement of AD.

LPS induces endogenous antimicrobials in the epidermis

(*1) Immunopotentiator from Pantoea agglomerans Prevents Atopic Dermatitis Induced by Dermatophagoides farinae Extract in NC/Nga Mouse, Anticancer Research 35: 4501-4508 (2015)
(*2) Effects of nonpathogenic gram-negative bacterium Vitreoscilla filiformis lysate on atopic dermatitis: a prospective, randomized, double-blind, placebo-controlled clinical study, Br. J. Dermatol. 159: 1357-1363 (2008)
(*3) Atopic dermatitis and filaggrin, Current Opinion in Immunology 42: 1-8 (2016)
(*4) Propionibacterium acnes Activates the IGF-1/IGF-1R System in the Epidermis and Induces Keratinocyte Proliferation, J Invest Dermatol 13 : 59-66 (2011)
(*5) Dysbiosis and Staphylococcus aureus Colonization Drives Inflammation in Atopic Dermatitis, Immunity 42: 756-766 (2015)
(*6) Expressions of β-defensins in human keratinocyte cell lines, J dermatol Sci 27: 183-191 (2001)

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