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Bacterial cell membranes and keratinocytes represent a composite biological context rather than a single molecular target, typically discussed in the development of topical antimicrobial and wound-healing agents. The bacterial cell membrane is the primary therapeutic target for antibiotics like polymyxins and antimicrobial peptides (AMPs), which act by binding to negatively charged components such as lipopolysaccharides (LPS), leading to membrane permeabilization and cell death [PubChem, NIH]. Keratinocytes are the predominant cell type in the human epidermis and serve as the host environment for these treatments; they also play an active role in the innate immune response by producing endogenous AMPs like LL-37 [PubMed, PMID: 17581955]. In drug development, the interaction with keratinocytes is evaluated to ensure that antimicrobial agents are selective for microbial membranes over mammalian cell membranes, which are rich in zwitterionic phospholipids and cholesterol [Nature, 2002]. Furthermore, some agents targeting bacterial membranes also stimulate keratinocytes to migrate or release cytokines, thereby accelerating wound closure and modulating inflammation [Journal of Investigative Dermatology, 2007]. Consequently, this entry is considered incorrect as a single target because it combines a microbial structure with a host cell type, representing the interface between pathogen eradication and host tissue preservation.
Disruption of bacterial lipid bilayers through electrostatic interactions and pore formation, alongside the modulation of keratinocyte signaling pathways (e.g., via FPR2 or P2X7 receptors) to promote wound healing and innate immune responses.
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