BACKGROUND: Parotid secretory protein (PSP) is a major salivary protein that is thought to possess both antibacterial and anti-inflammatory activity. A major question is whether PSP expression can be regulated by humoral factors and bacteria. Periodontitis is an inflammatory lesion initiated by interaction between gingival keratinocytes and periodontopathogenic microorganisms such as the Gram-negative anaerobe Porphyromonas gingivalis. Cytokines and sex hormones have been implicated in the progression of various forms of periodontal diseases. MATERIALS AND METHODS: We investigated the expression of PSP and its regulation in primary cultures of human gingival keratinocytes (HGK). HGK at the third or fourth passage were exposed to heat-killed P. gingivalis, tumor necrosis factor-alpha (TNF-alpha) and 17beta-estradiol. The PSP mRNA levels were examined by real-time polymerase chain reaction (PCR). The protein expression of PSP was confirmed by immunofluorescence. RESULTS: Heat-killed P. gingivalis, TNF-alpha and 17beta-estradiol all resulted in increased HGK levels of mRNA for PSP as determined by real-time PCR analysis. Immunofluorescence demonstrated increased PSP localized within the cytoplasm of HGK following exposure to killed P. gingivalis. CONCLUSION: The present study has demonstrated for the first time that PSP is expressed in keratinocytes and that it can be up-regulated by bacteria and humoral factors. Thus PSP may have a role in the innate defense system at the gingival epithelial surface. Copyright (c) Blackwell Munksgaard 2005.
BACKGROUND:Parotid secretory protein (PSP) is a major salivary protein that is thought to possess both antibacterial and anti-inflammatory activity. A major question is whether PSP expression can be regulated by humoral factors and bacteria. Periodontitis is an inflammatory lesion initiated by interaction between gingival keratinocytes and periodontopathogenic microorganisms such as the Gram-negative anaerobe Porphyromonas gingivalis. Cytokines and sex hormones have been implicated in the progression of various forms of periodontal diseases. MATERIALS AND METHODS: We investigated the expression of PSP and its regulation in primary cultures of human gingival keratinocytes (HGK). HGK at the third or fourth passage were exposed to heat-killed P. gingivalis, tumor necrosis factor-alpha (TNF-alpha) and 17beta-estradiol. The PSP mRNA levels were examined by real-time polymerase chain reaction (PCR). The protein expression of PSP was confirmed by immunofluorescence. RESULTS: Heat-killed P. gingivalis, TNF-alpha and 17beta-estradiol all resulted in increased HGK levels of mRNA for PSP as determined by real-time PCR analysis. Immunofluorescence demonstrated increased PSP localized within the cytoplasm of HGK following exposure to killed P. gingivalis. CONCLUSION: The present study has demonstrated for the first time that PSP is expressed in keratinocytes and that it can be up-regulated by bacteria and humoral factors. Thus PSP may have a role in the innate defense system at the gingival epithelial surface. Copyright (c) Blackwell Munksgaard 2005.
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