The survival of a multicellular organism in a world laden with microorganisms depends on a network of host defense mechanisms involving several levels of interacting systems. Microbial compound-induced production of antimicrobial peptides leads to the elimination of skin-infecting pathogens. In atopic dermatitis, a chronic inflammatory skin disease, this defense mechanism seems to be blocked. Keratinocytes play a key initiating role in cutaneous immune response against pathogen. Keratinocytes have been shown to recognize a wide variety of microorganisms through their TLRs. Signaling through specific TLR combinations provides selectivity and specificity to keratinocyte immune responses. TLR-mediated signaling pathways induce the production of proinflammatory cytokines, chemokines, inducible enzymes and antimicrobial peptides in epidermal keratinocytes.

Interaction of AMPs with cell-surface receptors turns results in effects on intracellular signaling pathways. AMPs have also been shown to interact with Toll-like receptors (TLRs) signaling in the adaptive immune response through interaction with the cellular membrane and epidermal growth factor receptor. Finally, AMPs are known to act synergistically with endogenous inflammatory mediators. As a result of these many and complex interactions, AMPs increase cell migration and chemokine secretion.

Keratinocyte-derived cytokines and chemokines are critical in the recruitment of dendritic cells, T cells, and neutrophils into the sites of infection. In addition to their primary functions, antimicrobial peptides can act as chemokines, while chemokines can act as antimicrobial compounds at sites of infection, thereby providing a more effective immune response against pathogens. In addition, these proinflammatory cytokines have direct effects on AMP production and are also crucial for the activation of the adaptive immune response.

Langerhans cells are recognized as the major antigen-presenting cells of the skin and play a key role as the peripheral component of the immune system. They have long dendrites (like arms) that capture antigen in the skin, and when they find an antigen, they migrate to lymph nodes and present to T cells allowing the adaptive immune system to respond.

Keratinocytes play a role in initiating cell-mediated immune responses in the skin by releasing cytokines and expressing cellular adhesion molecules to facilitate the movement of immune competent cells. The adaptive immune system consists of cells that recognize specific foreign substances and act to neutralize or destroy them. Once the innate immune barrier has been breached, adaptive immunity is the last barrier to pathogen entry. There is considerable overlap between the innate and adaptive immune responses, which work in concert to eliminate or neutralize invading pathogens.

Common disorders such as dry skin, psoriasis, atopic dermatitis, acne and rosacea are all related to skin barrier dysfunction. Epidermal barrier dysfunction is pathologically involved in a variety of common, antigen-driven skin diseases. Skin barrier dysfunction allows epicutaneous penetration of allergens, leading to increased skin infections and inflammatory responses which continue to drive the allergic process. Given the complexity and clinical heterogeneity of this disorder, it is likely that a combination of these factors is responsible for the pathogenesis of this disease.

·Evaluation of the anti-inflammatory and atopic dermatitis-mitigating effects of BSASM, a multicompound preparation. Journal of ethnopharmacology, 2005, 96, 211-219.

·In vitro antibacterial and anti-inflammatory effects of honokiol and magnolol against Propionibacterium sp. European Journal of Pharmacol, 2004, 2;496 (1-3),189-195.

·Registration No.: 10-0812596-0000; Registration Date: 05. Mar. 2008.

·Registration No.:10-0782599-0000; Registration Date: 07. Nov. 2007.

·MultiExBSASM, HerbEx Centella, MultiEx Naturotics, MultiEx Magnotics.