LPS activates the autophagy of the keratinocytes and the resultant control of their turnover.
As mentioned in the section on "Structure of the skin,” in the epidermis, new keratinocytes born at the lowest part are pushed upwards while undergoing morphological changes. When they age at the top, they peel off. The replacement of all the epidermal cells with new ones is called turnover. On healthy skin, the turnover occurs about once a month. In order for the turnover to be successful, it is important that the keratinocytes change their morphology, that is, differentiate, correctly.
The mechanism of “autophagy” is deeply involved in the differentiation of keratinocytes. The study of autophagy was awarded the Nobel Prize in Medicine and Physiology in 2016. Autophagy is a mechanism of the degradation of intracellular proteins. Keratinocytes change the insides of the cells via autophagy. In the keratinocytes, autophagy is involved not only in turnover but also in melanin degradation and infection prevention (*1).
In fact, LPS is known to promote autophagy in macrophages and keratinocytes (*2, 3). The figure below shows that the expression level of LC3 (Microtubule-associated protein light chain 3), a marker of autophagy, increases when human keratinocyte cell lines are treated with LPS. Thus, it is believed that the action of LPS on the skin also contributes to the promotion of epidermis turnover.
(*1)The signaling involved in autophagy machinery in keratinocytes and therapeutic approaches for skin diseases, Oncotarget 7 (31): 50682-50697 (2016)
(*2)Toll-like Receptor 4 Is a Sensor for Autophagy Associated with Innate Immunity, Immunity 27: 135-144 (2007)
(*3)Lipopolysaccharide induces bacterial autophagy in epithelial keratinocytes of the gingival sulcus, BMC Cell Biology 19:18 (2018)
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