Altered free cytosolic calcium changes and neutrophil chemotaxis in patients with juvenile periodontitis

Agarwal, Sudha; Reynolds, M. A.; Duckett, Laura; Suzuki, Jon B.

doi:10.1111/j.1600-0765.1989.tb00870.x

Cited by 39 publications

(17 citation statements)

References 26 publications

(25 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In these families, the neutrophil abnormality relating to reduced chemotaxis has been well characterized by a number of laboratories. This includes decreased chemotaxis to a number of chemotactic factors associated with reduced receptor expression on the neutrophil surface for those chemotactic factors (Van Dyke et al 1981), reduced calcium transport in LAP neutrophils (Agarwal et al 1989), increased diacylglycerols levels in stimulated LAP neutrophils, and decreased protein kinase C activity (Kurihara et al 1993). The finding that these observations are not universal in the LAP populations reported in different geographic locations, or even within the same geographic population, strongly supports the hypothesis that there are several distinct forms of disease with the same clinical presentation.…”

Section: Introductionmentioning

confidence: 98%

Localized aggressive periodontitis is linked to human chromosome 1q25

Hastürk

et al. 2003

Hum Genet

View full text Add to dashboard Cite

Localized aggressive periodontitis (LAP; previously known as localized juvenile periodontitis) is one of the rapidly progressive periodontal diseases. Certain forms of familial LAP show a simple Mendelian pattern of transmission. However, no gene mutation has been identified to be responsible for the LAP phenotype. As an initial step to identify a gene mutation associated with LAP, we have performed genetic linkage analysis with four multigenerational families exhibiting the LAP phenotype. Affected individuals in the families were identified based on clinical and laboratory criteria in an attempt to define a homogeneous phenotype, since the clinical presentation of LAP may represent a manifestation of a heterogeneous group of diseases. The LAP phenotype is linked to a DNA marker, D1S492, with LOD score 3.48, theta=0.00. The haplotype analysis of the chromosome interval associated with D1S492 indicates that a LAP locus is located between D1S196 and D1S533 on chromosome 1, covering about 26 million DNA basepairs. We have also examined the DNA sequence of prostaglandin-endoperoxide synthase 2 (PTGS2 or cyclooxygenase 2, COX2) since prostaglandin 2 (PGE2), the product of COX2, is upregulated in LAP patients and COX2 is located between D1S196 and D1S533. No mutation in COX2 was identified in the patients.

show abstract

Section: Introductionmentioning

confidence: 98%

Localized aggressive periodontitis is linked to human chromosome 1q25

Hastürk

et al. 2003

Hum Genet

View full text Add to dashboard Cite

show abstract

“…This was due to decreased Ca 2+ influx. These reduced [Ca 2+ ] i levels were associated with reduced PKC levels and defective chemotaxis [40,41]. Similarly in aged individuals, PMNL showed low [Ca 2+ ] i levels that were associated with defective chemotaxis and oxidative burst [42].…”

Section: Discussionmentioning

confidence: 99%

Altered Ca2+ homeostasis in polymorphonuclear leukocytes from chronic myeloid leukaemia patients

2006

View full text Add to dashboard Cite

Background: In polymorphonuclear leukocytes (PMNL), mobilization of calcium ions is one of the early events triggered by binding of chemoattractant to its receptors. Besides chemotaxis, a variety of other functional responses are dependent on calcium ion mobilization. PMNL from chronic myeloid leukaemia (CML) patients that were morphologically indistinguishable from normal PMNL were found to be defective in various functions stimulated by a chemoattractant -fMLP. To study the mechanism underlying defective functions in CML PMNL, we studied calcium mobilization in CML PMNL in response to two different classical chemoattractants, fMLP and C5a.

show abstract

“…The most consistent abnormality in host response in patients with LJP is the depressed in vitro chemotaxis of peripheral blood neutrophils, first described over 20 years ago (8,9,19,(22)(23)(24)(25)(26)(27)(28)(29). Subsequently, in vivo tests have confirmed the in vitro results (30)(31)(32).…”

Section: Chemotaxismentioning

confidence: 90%

A Potential Role of an Intracellular Signaling Defect in Neutrophil Functional Abnormalities and Promotion of Tissue Damage in Patients with Localized Juvenile Periodontitis

Leino¹,

Hurttia²

1999

CCLM

View full text Add to dashboard Cite

Localized juvenile periodontitis is a destructive form of periodontal inflammatory disease which has its onset at puberty. The etiopathology of the disease is still unclear but neutrophils have been suggested to play a major role both in the production and development of the disorder. About 70% of the patients with localized juvenile periodontitis exhibit neutrophil functional abnormalities, such as decreased chemotaxis and phagocytosis. Interestingly, it has been frequently reported that the same hypoactive cells show an enhanced respiratory burst response and increased adhesion. Several possible mechanisms explaining neutrophil anomalies in localized juvenile periodontitis have been proposed. These include the presence of soluble serum factors capable of modulating neutrophil function, altered cell-surface receptor expression and/or function, and a change in the post-receptor signaling events. Recently, a growing evidence has accumulated showing that the diacylglycerol metabolism could be altered in neutrophils from patients with localized juvenile periodontitis. This change, which may be due to a defect in a major diacylglycerol metabolizing enzyme, diacylglycerol kinase, results in enhanced accumulation of diacylglycerol in activated cells. Because diacylglycerol is an endogenous activator of protein kinase C, the increased and prolonged generation of diacylglycerol could lead to abnormal pattern of protein kinase C-regulated neutrophil functions, explaining the parallel hypo- and hyperactivities.

show abstract

Altered free cytosolic calcium changes and neutrophil chemotaxis in patients with juvenile periodontitis

Cited by 39 publications

References 26 publications

Localized aggressive periodontitis is linked to human chromosome 1q25

Localized aggressive periodontitis is linked to human chromosome 1q25

Altered Ca2+ homeostasis in polymorphonuclear leukocytes from chronic myeloid leukaemia patients

A Potential Role of an Intracellular Signaling Defect in Neutrophil Functional Abnormalities and Promotion of Tissue Damage in Patients with Localized Juvenile Periodontitis

Contact Info

Product

Resources

About