Antimicrobial peptides (AMPs) are small molecular weight proteins with broad spectrum antimicrobial activity against bacteria, viruses, and fungi. These evolutionarily conserved peptides are usually positively charged and have both a hydrophobic and hydrophilic side that enables the molecule to be soluble in aqueous environments yet also enter lipid-rich membranes. Once in a target microbial membrane, the peptide kills target cells through diverse mechanisms. Cathelicidins and defensins are major groups of epidermal AMPs. Decreased levels of these peptides have been noted for patients with atopic dermatitis and Kostmann's syndrome, a congenital neutropenia. In addition to important antimicrobial properties, growing evidence indicates that AMPs alter the host immune response through receptor-dependent interactions. AMPs have been shown to be important in such diverse functions as angiogenesis, wound healing, and chemotaxis. As our knowledge of AMP biology expands, the precise role and relevance of these peptides will be better elucidated.

Human intestinal epithelial cells secrete an array of chemokines known to signal the trafficking of neutrophils and monocytes important in innate mucosal immunity. We hypothesized that intestinal epithelium may also have the capacity to play a role in signaling host adaptive immunity. The CC chemokine macrophage inflammatory protein (MIP)-3alpha/CCL20 is chemotactic for immature dendritic cells and CD45RO(+) T cells that are important components of the host adaptive immune system. In these studies, we demonstrate the widespread production and regulated expression of MIP-3alpha by human intestinal epithelium. Several intestinal epithelial cell lines were shown to constitutively express MIP-3alpha mRNA. Moreover, MIP-3alpha mRNA expression and protein production were upregulated by stimulation of intestinal epithelial cells with the proinflammatory cytokines tumor necrosis factor-alpha or interleukin-1alpha or in response to infection with the enteric bacterial pathogens Salmonella or enteroinvasive Escherichia coli. In addition, MIP-3alpha was shown to function as a nuclear factor-kappaB target gene. In vitro findings were paralleled in vivo by increased expression of MIP-3alpha in the epithelium of cytokine-stimulated or bacteria-infected human intestinal xenografts and in the epithelium of inflamed human colon. Mucosal T cells, other mucosal mononuclear cells, and intestinal epithelial cells expressed CCR6, the cognate receptor for MIP-3alpha. The constitutive and regulated expression of MIP-3alpha by human intestinal epithelium is consistent with a role for epithelial cell-produced MIP-3alpha in modulating mucosal adaptive immune responses.

Propranolol is a relatively recent therapy of hemangiomas with fewer side effects, a different mechanism of action, and greater efficacy than current first-line corticosteroid therapy. Many of these studies do not have the same patient population or duration/regimen of treatment for hemangiomas; however, based on available data in the literature, it appears that propranolol could be an emerging and effective treatment for infantile hemangiomas. Further randomized controlled trials are recommended.