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Expression of LL-37 by human gastric epithelial cells as a potential host defense mechanism against Helicobacter pylori
Ist Teil von
Gastroenterology (New York, N.Y. 1943), 2003-12, Vol.125 (6), p.1613-1625
Ort / Verlag
United States: Elsevier Inc
Erscheinungsjahr
2003
Quelle
MEDLINE
Beschreibungen/Notizen
Background & Aims
:
LL-37/human cationic antimicrobial peptide 18 (hCAP18) is a human cathelicidin with broad-spectrum antimicrobial, lipopolysaccharide binding, and chemotactic activities. This study examined the role of LL-37/hCAP18 in gastric innate immune defense by characterizing its constitutive and regulated expression by human gastric mucosa and its bactericidal activity against the gastric pathogen
Helicobacter pylori.
Methods
:
LL-37/hCAP18 messenger RNA expression in normal and
H. pylori-infected gastric mucosa and gastric epithelial cells was determined by in situ hybridization, real-time polymerase chain reaction, immunostaining, and immunoblot analysis. Bactericidal activity was measured by using a colony-forming unit assay.
Results
:
LL-37/hCAP18 messenger RNA and protein were expressed in a distinct distribution by surface epithelial cells as well as chief and parietal cells in the fundic glands of normal gastric mucosa. LL-37/hCAP18 was significantly increased in the epithelium and gastric secretions of
H. pylori-infected patients, but not in individuals with non-
H. pylori-induced gastric inflammation. Infection of cultured gastric epithelial cells with a wild-type but not an isogenic ΔcagE mutant strain of
H. pylori increased LL-37/hCAP18 expression, indicating that
H. pylori-induced regulation of LL-37/hCAP18 production required an intact type IV secretion system. LL-37, the C-terminal peptide of LL-37/hCAP18, alone or in synergy with human β-defensin 1, was bactericidal for several
H. pylori strains.
Conclusions
:
These data indicate that
H. pylori up-regulates production of LL-37/hCAP18 by gastric epithelium and suggest this cathelicidin contributes to determining the balance between host mucosal defense and
H. pylori survival mechanisms that govern chronic infection with this gastric pathogen.