title: Defective calcium influx factor activity in neutrophils from patients with localized juvenile periodontitis.
abstract: BACKGROUND
  Localized juvenile periodontitis (LJP) is an early-onset periodontal disease associated with neutrophil dysfunction, including defective chemotaxis, reduced protein kinase C (PKC) activity, and reduced calcium entry. These observations are important because reduced availability of cytosolic-free calcium concentration in the cell will have detrimental consequences for the numerous cytosolic calcium concentration-dependent pathways. In particular, there is a direct relationship between Ca2+ flux and the cell activation enzyme PKC. In this report, we focused on the mechanism of calcium entry, investigating a newly described molecule, calcium influx factor (CIF). CIF is thought to be a second messenger for the opening of membrane calcium channels when intracellular calcium stores are depleted. We examined CIF activity in neutrophils from normal subjects and LJP patients.
  
  
  METHODS
  Neutrophils from 11 LJP patients, 3 adult periodontitis (AP) patients, and 12 normal subjects were isolated from peripheral venous blood. CIF was extracted with thapsigargin, a Ca2+-ATPase inhibitor, from isolated neutrophils and CIF activity measured using a 45CaCl2 uptake assay.
  
  
  RESULTS
  The CIF activity in neutrophils from LJP patients ranged from 98.9 to 281.5 units/mg protein (mean = 180.2 +/- 56.3) and from 291.9 to 755.5 units/mg protein (mean = 528.8 +/- 153.8) in non-periodontal disease controls. CIF activity in AP patients was also measured and found to be similar to controls. The CIF activity in LJP patients was statistically significantly reduced compared to that in normal subjects (P <0.001).
  
  
  CONCLUSIONS
  This study suggests that CIF activity may be an important determinant in neutrophil abnormalities in LJP.
authors.affiliation: Department of Periodontology and Oral Biology, Boston University Goldman School of Dental Medicine, MA 02118, USA. kshiba@bu.edu
authors.forename: K
authors.initials: K
authors.lastname: Shibata
authors.forename: M L
authors.initials: ML
authors.lastname: Warbington
authors.forename: B J
authors.initials: BJ
authors.lastname: Gordon
authors.forename: H
authors.initials: H
authors.lastname: Kurihara
authors.forename: T E
authors.initials: TE
authors.lastname: Van Dyke
mesh_terms: D000293:Adolescent; D000328:Adult; D010520:Aggressive Periodontitis / Q000097:blood / Q000276:immunology / Q000378:metabolism*; D000704:Analysis of Variance; D001685:Biological Factors / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism*; D002120:Calcium Channel Agonists / Q000378:metabolism*; D020013:Calcium Signaling; D016022:Case-Control Studies; D002634:Chemotaxis, Leukocyte; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000378:metabolism; D010518:Periodontitis / Q000097:blood / Q000276:immunology / Q000378:metabolism; D011493:Protein Kinase C / Q000378:metabolism; D015290:Second Messenger Systems; D018709:Statistics, Nonparametric
chemical_list: D001685:Biological Factors; D002120:Calcium Channel Agonists; D011493:Protein Kinase C; D002118:Calcium