Archives of ophthalmology (Chicago, Ill. : 1960) · 2012
Regulation of leukotriene B4 secretion by human corneal, conjunctival, and meibomian gland epithelial cells.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Sahin Afsun, Kam Wendy R, Darabad Raheleh Rahimi, Topilow Kimberly, Sullivan David A
Аннотация
OBJECTIVES: To test the hypotheses that lipopolysaccharide (LPS) stimulates leukotriene B4 (LTB4) production in human ocular surface and adenexal cells, arachidonic acid duplicates the stimulatory effect of LPS, LPS-binding protein potentiates LPS-induced LTB4 secretion, and dihydrotestosterone attenuates the immune effect of LPS.
METHODS: Immortalized human corneal, conjunctival, and meibomian gland epithelial cells were cultured in the presence or absence of fetal bovine serum and were exposed to vehicle, LPS, LPS plus LPS-binding protein, arachidonic acid, or dihydrotestosterone. Culture media were processed for the LTB4 analysis.
RESULTS: Lipopolysaccharide stimulates time-dependent secretion of LTB4 by human corneal, conjunctival, and meibomian gland epithelial cells. This effect, which we could not detect with arachidonic acid, is potentiated by exposure to LPS-binding protein. This potentiation, in turn, is significantly reduced by cellular treatment with dihydrotestosterone.
CONCLUSIONS: Ocular epithelial cells have the ability to generate LTB4 in response to LPS exposure. This proinflammatory process is modulated by LPS-binding protein and by dihydrotestosterone.
CLINICAL RELEVANCE: When induced by appropriate stimuli, LTB4 production may have a role in the generation of inflammation in ocular surface disease.
METHODS: Immortalized human corneal, conjunctival, and meibomian gland epithelial cells were cultured in the presence or absence of fetal bovine serum and were exposed to vehicle, LPS, LPS plus LPS-binding protein, arachidonic acid, or dihydrotestosterone. Culture media were processed for the LTB4 analysis.
RESULTS: Lipopolysaccharide stimulates time-dependent secretion of LTB4 by human corneal, conjunctival, and meibomian gland epithelial cells. This effect, which we could not detect with arachidonic acid, is potentiated by exposure to LPS-binding protein. This potentiation, in turn, is significantly reduced by cellular treatment with dihydrotestosterone.
CONCLUSIONS: Ocular epithelial cells have the ability to generate LTB4 in response to LPS exposure. This proinflammatory process is modulated by LPS-binding protein and by dihydrotestosterone.
CLINICAL RELEVANCE: When induced by appropriate stimuli, LTB4 production may have a role in the generation of inflammation in ocular surface disease.