Premium
Altered free cytosolic calcium changes and neutrophil chemotaxis in patients with juvenile periodontitis
Author(s) -
Agarwal S.,
Reynolds M. A.,
Duckett L. D.,
Suzuki J. B.
Publication year - 1989
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.1989.tb00870.x
Subject(s) - chemotaxis , neutrophile , cytosol , n formylmethionine leucyl phenylalanine , calcium , medicine , endocrinology , intracellular , stimulation , chemistry , calcium in biology , granulocyte , immunology , inflammation , biochemistry , enzyme , receptor
Nearly 70–75% of patients with localized juvenile periodontitis (JP) have abnormal polymorphonuclear leukocytic (PMN) chemotaxis. The objective of this study was to determine whether the lower chemotactic response in PMNs from JP patients is associated with a defect in intracellular signal transduction, as measured by stimulus‐induced changes in free cytosolic calcium (Ca 2+ ) mobilization. We report that peptide chemoattractants such as N‐formyl‐methionyl‐leucyl‐phenylalanine (fMLP) and the complement fragment C 5a in direct comparative studies induced lower amounts of initial Ca 2+ mobilization in PMNs from JP patients than healthy controls, as monitored by intracellular fura‐2 fluorescence. The initial resting levels of free cytosolic Ca 2+ in PMNs from JP patients and normal individuals were found to be similar. fMLP and C 5a both mobilized Ca 2+ in PMNs in a dose‐dependent manner. Treatment of PMNs from 0.16 to 20 nM fMLP and 0.2 to 20 nM C 5a resulted in elevated levels of free cytosolic Ca 2+ . However, above 20 nM fMLP and 5 nM C 5a concentrations the extent of total Ca 2+ mobilization did not differ significantly. Although fMLP and C 5a caused Ca 2+ mobilization in PMN cells from JP and healthy control subjects, fMLP stimulation induced higher levels of free cytosolic Ca 2+ mobilization in PMN cells from healthy control subjects (141.29 ± 25.55 nM/ 2 ± 10 6 PMNs), than PMNs from JP patients (62.33 ± 23.76 nM/2 ± 10 6 PMNs). Similarly C 5a induced higher levels of Ca 2+ mobilization in PMNs from healthy control individuals (130.43 ± 18.26 nM Ca 2+ /2 ± 10 6 PMNs), when compared to JP patients (49.92 ± 14.92 nM Ca 2+ /2 ± 10 6 PMNs). JP patients also exhibited significantly lower chemotaxis towards fMLP (74.51 ± 6.31%) and C 5a (69.25 ± 5.44%) as compared to healthy control subjects. The data suggest that PMNs from JP patients exhibit an intrinsic anomaly in the mechanism(s) responsible for intracellular Ca 2+ mobilization which correlates with a PMN chemotactic defect.