Rosacea is a chronic multifactor dermatosis, realized by pathological reaction of blood vessels under the influence of vasoactive peptides, antibodies, circulating immune complexes and characterized by recurrent course, stages and manifested by hyperemia of the face, papules, pustules, telangioectasia, hyperplasia of the sebaceous glands and connective tissue [1]. A key role in the pathogenesis of rosacea plays a cutaneous inflammatory process. Inflammation is initiated with the participation of TLR2 (Toll-like receptor, toll-like receptors) keratinocytes. These transmembrane structures can be activated by physical factors (UFO, high and low temperatures), a number of antigens (chitin shell D. folliculorum, glycoproteins B. Oleronius; in dermal infiltrates in the area of lesions found T-lymphocytes sensitized to antigens D. folliculorum), neuropeptides during stress (neuroimmune mechanisms) or the formation of viscerocutaneous reflexes. Further development of inflammation due to the secretion by the keratinocytes of inflammatory proteases (matrix metalloproteinases, kallikreins) and antimicrobial peptides (alpha-, betadefensins and cathelicidin LL-37). Currently, it is the cathelicidin LL-37 plays a significant role in the development of rosacea. This antimicrobial polypeptide, consisting of 37 amino acids, belongs to the family kallikrein-kinin. Its level in the affected skin is significantly increased in all subtypes of rosacea. Products LL-37 is enhanced by the influence of UFO (due to the synthesis of vitamin D), high and low temperatures, infectious agents. Intradermal injections of LL-37 cause the development of dermatitis clinically similar to rosacea in experimental animals [2].