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Polyamines Found in the Inflamed Periodontium Inhibit Priming and Apoptosis in Human Polymorphonuclear Leukocytes
Author(s) -
Ratasirayakorn Waraporn,
Leone Peter,
Leblebicioglu Binnaz,
Walters John D.
Publication year - 1999
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.1999.70.2.179
Subject(s) - spermidine , apoptosis , acridine orange , putrescine , dna fragmentation , microbiology and biotechnology , respiratory burst , programmed cell death , superoxide , cytochrome c , tumor necrosis factor alpha , andrology , chemistry , biology , immunology , biochemistry , medicine , enzyme
Background: Polymorphonuclear leukocytes (PMNs) are exposed to high concentrations of polyamines in the inflamed periodontium and possess a transport system for taking up these compounds. Previous studies suggest that polyamines are involved in priming of the PMN respiratory burst by tumor necrosis factor‐α (TNF‐α) and can stabilize DNA against degradation. The purpose of this study was to determine whether exogenous polyamines can modulate priming by TNF‐α or delay nuclear changes associated with PMN apoptosis (programmed cell death). Methods: Isolated human PMNs were incubated with putrescine or spermidine in vitro. Superoxide generation was measured with a cytochrome C reduction assay, and apoptotic changes were assessed by fluorescence microscopy (after cell staining with acridine orange and ethidium bromide). Results: Incubation with 1 mM putrescine for 1 hour inhibited superoxide production by TNF‐primed PMNs by 20%, but enhanced the production of superoxide by unprimed cells by 38%. Both effects were dose dependent and statistically significant ( P <0.03, repeated measures ANOVA and Dunnett's test). Spermidine had no significant effects on PMN oxidative function. With regard to apoptosis, 1 mM putrescine or spermidine produced a statistically significant reduction in the proportion of apoptotic PMNs within 6 to 9 hours ( P <0.05). In cells incubated for 7 hours with 300 µM putrescine or spermidine, the proportion of apoptotic cells was approximately 30% lower than in untreated controls ( P <0.05, Dunnett's test). The delay of apoptosis by spermidine was less profound than that produced by TNF‐α and was not additive to the effects of this cytokine. Conclusions: Polyamines could potentially impair the priming of PMN oxidative function by TNF‐α at sites where this cytokine is present. In the absence of TNF‐α, polyamines could enhance PMN superoxide release and enhance the maintenance of PMN function in the periodontal pocket. J Periodontol 1999;70:179‐184.