The Molecular Basis for Neutrophil Dysfunction in Early‐Onset Periodontitis

Nardin, Ernesto De

doi:10.1902/jop.1996.67.3s.345

Cited by 12 publications

(13 citation statements)

References 100 publications

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“…Recently, we have reported that a number of dierentially displayed bands were obtained from human neutrophils stimulated with LPS from P. gingivalis (6). Other researchers have also shown that stimulated neutrophils have an ability to express a number of transcripts (1,26). To assess dierences in susceptibility of neutrophils between the dierent patient groups and healthy subjects, we have utilized a single dose of FMLP for RAP-PCR analyses.…”

Section: Discussionmentioning

confidence: 99%

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Differential gene expression in neutrophils from patients with generalized aggressive periodontitis

Kubota

Morozumi

Shimizu

et al. 2001

J of Periodontal Research

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Differential gene expression was investigated in neutrophils stimulated with N-formyl-methionyl-leucyl-phenylalanine using RNA fingerprinting by arbitrarily primed polymerase chain reaction (RAP-PCR). The cells were isolated from 3 groups of subjects: patients with generalized aggressive periodontitis (Aggressive-P. n = 6), generalized chronic periodontitis (Chronic-P, n = 6) and healthy controls (H, n = 8). Our results show that 37 genes were upregulated. while 27 genes were down-regulated in all Aggressive-P neutrophils by using RAP-PCR with 45 primer pairs. Reverse transcription-PCR analyses revealed that mRNA levels were significantly different (p<0.05) for heat shock transcription factor 4b (HSF4b) gene. Kruppel-like zinc finger transcription factor 9 (Zf9) and muskelin genes. HSF4b was greater in neutrophils from Aggressive-P compared to groups H and Chronic-P. Zf9 and muskelin genes were lower in Aggressive-P compared to the H groups, but no significant difference was noted compared to the Chronic-P group. The control genes, IL-1beta and VEGF genes, were expressed at a significantly higher level in Aggressive-P and Chronic-P than H (p<.01, p<0.05). In conclusion, the RAP-PCR technique used in this study enabled us to identify 3 Aggressive-P related genes, which had not been reported previously. Neutrophil functions in Aggressive-P patients are suggested to be altered by regulatory factors of the immune system including HSF4b (transcription factor), Zf9 (activator of TGF-beta) and muskelin (cellular adhesion).

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Section: Discussionmentioning

confidence: 99%

“…This reduction of muskelin expression in Aggressive-P neutrophils suggests the decline of cellular energy metabolism. The level of muskelin expression might be associated with the neutrophil dysfunction known to exist in Aggressive-P, such as adhesive and cytoskeletal metabolism following bacterial challenge (1,3,36).…”

Section: Discussionmentioning

confidence: 99%

Differential gene expression in neutrophils from patients with generalized aggressive periodontitis

Kubota

Morozumi

Shimizu

et al. 2001

J of Periodontal Research

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“…Any factor that could suppress recruitment of PMN to infected areas, as well as the activation of PMN, may increase the susceptibility to infection. Numerous studies have demonstrated that severe and rapid periodontal breakdown may be associated with defective PMN function, more specifically with the chemotaxis of these cells (De Nardin 1996). The literature has been controversial on whether chemotaxis of the PMNs from PLS patients is depressed.…”

Section: Discussionmentioning

confidence: 99%

Leukocyte functions in 2 cases of Papillon‐Lefèvre syndrome

Liu

Cao

Meng

et al. 2000

J Clinic Periodontology

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“…Infections caused by A. actinomycetemcomitans are not resolved by the host response despite the accumulation of neutrophils at the site of inflammation (Attström and Egelberg, 1970; Attström, 1971). Neutrophil abnormalities such as neutropenia, depressed neutrophil chemotaxis and decreased phagocytic and bactericidal activities, have been associated with aggressive periodontitis (De Nardin, 1996; Dennison and van Dyke, 1997; Landi et al ., 1997). However, neutrophil dysfunctions have not been observed in all patients (Pedersen, 1988; Repo et al ., 1990; Mouynet et al ., 1994).…”

Section: Introductionmentioning

confidence: 99%

Resistance of fluorescent-labelled Actinobacillus actinomycetemcomitans strains to phagocytosis and killing by human neutrophils

2006

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SummaryNeutrophils are initially the predominant cells involved in the host defence of bacterial infections, including periodontal disease. Aggressive periodontitis is associated with Actinobacillus actinomycetemcomitans , a Gram-negative capnophilic microorganism. Infections caused by A. actinomycetemcomitans are not resolved by the host immune response despite the accumulation of neutrophils at the site of inflammation. To better understand the role of natural host defence mechanisms in A. actinomycetemcomitans infections, the interaction of phenotypically diverse strains of this pathogen with human neutrophils was assessed directly using techniques such as genetic labelling with the gene for green fluorescent protein, fluorescence-activated cell sorting and fluorescence imaging. The study included clinical isolates of A. actinomycetemcomitans represented by self-aggregating, biofilm-associated and isogenic planktonic variants. Data obtained showed that complement-mediated phagocytosis of A. actinomycetemcomitans was generally inefficient regardless of strain-specific serotype or leukotoxin production. Furthermore, the majority of ingested bacteria remained viable after exposure to neutrophils for 1 h. Interestingly, uptake of antibodyopsonized bacteria resulted in the rapid cell death of neutrophils. This was in contrast to ingestion of complement-opsonized bacteria, which did not affect neutrophil viability. The methods used in this study provided reliable and reproducible results with respect to adherence, phagocytosis and killing of A. actinomycetemcomitans when encountering human neutrophils.

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The Molecular Basis for Neutrophil Dysfunction in Early‐Onset Periodontitis

Cited by 12 publications

References 100 publications

Differential gene expression in neutrophils from patients with generalized aggressive periodontitis

Differential gene expression in neutrophils from patients with generalized aggressive periodontitis

Leukocyte functions in 2 cases of Papillon‐Lefèvre syndrome

Resistance of fluorescent-labelled Actinobacillus actinomycetemcomitans strains to phagocytosis and killing by human neutrophils

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