Bacterial products increase expression of the human cathelicidin hCAP-18/LL-37 in cultured human sinus epithelial cells

Abstract

The respiratory epithelium plays a major role in the primary defense of the airways against infection. It has been demonstrated that bacterial products are involved in the induction of inflammatory reactions of the upper airways. Little is known about the effects of bacterial products on expression of the antimicrobial peptide hCAP-18/LL-37, the only human cathelicidin identified so far. The aim of this study was to investigate the effects of bacterial products from both gram-positive and gram-negative bacteria on the expression of hCAP-18/LL-37 by sinus epithelial cells using an air-exposed tissue culture model. Lipopolysaccharide and lipoteichoic acid both increased hCAP-18/LL-37 expression in cultured sinus epithelium as assessed by immunohistochemistry, where maximal stimulation occurred at 100 ng ml(-1) lipopolysaccharide or 10 microg ml(-1) lipoteichoic acid. The stimulatory effect of lipopolysaccharide and lipoteichoic acid was not restricted to expression of hCAP-18/LL-37, since also mucin expression and IL-8 release from cultured sinus epithelium cells were increased by lipopolysaccharide and lipoteichoic acid. This suggests that bacterial products may stimulate innate immunity in the upper airways.

Expression of cathelicidin in recurrent throat infection

“…These bacterial effects on LL-37 expression were suggested to be mediated via bacterial DNA [17]. Nell et al demonstrated the increased expression of cathelicidin in nasal sinus epithelium in inflammation and the relationship with inflammation via stimulation of IL-8 released by epithelial cells [18]. In this study, we demonstrated that the chronic tonsillar inflammation upregulates the expression of cathelicidin in tonsillar epithelium.…”

Augmentation of Epithelial Resistance to Invading Bacteria by Using mRNA Transfections

“…CAMP expression can be induced by 1,25-dihydroxyvitamin D3 (13), pathogens (9), or lipopolysaccharide (LPS) (14). Decreased CAMP/LL-37 production accompanies increased invasion and colonization by pathogens in epithelial cells, which characterizes diseases such as morbus Kostmann (15) and atopic dermatitis (16).…”

Vitamin D-Mediated Induction of Innate Immunity in Gingival Epithelial Cells

“…In addition, it exhibits chemotactic properties and plays a role in dendritic cell maturation, identifying it as an important mediator in the innate and adaptive immune systems (reviewed in reference 6). LL-37 gene expression can be induced by live bacteria (36) or by bacterial products such as lipopolysaccharide (LPS) (30,39), and the active LL-37 peptide is processed from the inactive human CAP-18 (hCAP-18) precursor by proteolysis. Lack of LL-37 is associated with two human disorders, morbus Kostmann and Papillon-Lefèvre syndrome, in which there is severe periodontal disease associated with colonization by the periodontal pathogen Aggregatibacter actinomycetemcomitans (8,11,41).…”

“…Lack of LL-37 is associated with two human disorders, morbus Kostmann and Papillon-Lefèvre syndrome, in which there is severe periodontal disease associated with colonization by the periodontal pathogen Aggregatibacter actinomycetemcomitans (8,11,41). LL-37 gene expression can be induced by live bacteria (36) or by bacterial products such as LPS (30,39), making the peptide part of the innate immune defense of the gingival epithelium.…”