Altered chemotactic behavior of crevicular PMNs in different forms of periodontitis

Sigusch, Bernd W.; Eick, Sigrun; Pfister, W.; Klinger, G; Glockmann, E

doi:10.1034/j.1600-051x.2001.028002162.x

Cited by 26 publications

(35 citation statements)

References 39 publications

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“…Consistent with previous studies, 3–6 PMNs from our AgP cases exhibited significantly decreased chemotaxis toward fMLF and reduced FPR1 expression relative to PMNs from controls. We observed a 19% to 22% decrease in chemotaxis activity, whereas previous investigations reported a decrease of ∼20% to 50%.…”

Section: Discussionsupporting

confidence: 92%

“…AgP is associated with invasive bacterial pathogens, such as Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans ) and Porphyromonas gingivalis. 1,2 In addition, polymorphonuclear leukocytes (PMNs) from individuals affected by AgP exhibit reduced binding of N‐formylpeptides and a significant reduction in chemotactic activity toward formylpeptides relative to PMNs from healthy control subjects 3–6 …”

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confidence: 99%

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Formylpeptide Receptor Single Nucleotide Polymorphism 348T>C and Its Relationship to Polymorphonuclear Leukocyte Chemotaxis in Aggressive Periodontitis

Maney

Walters

2009

Journal of Periodontology

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Background-Aggressive periodontitis (AgP) is associated with impaired polymorphonuclear leukocyte (PMN) chemotaxis toward bacterial N-formylpeptides. Formylpeptide receptors (FPRs) play a major role in guiding PMNs to infection sites. Previous work revealed a significant association between FPR1 single nucleotide polymorphism (SNP) 348T>C and AgP in African Americans. We tested the hypothesis that 348T impairs PMN chemotaxis by decreasing FPR mRNA expression, thereby increasing susceptibility to AgP.

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Section: Discussionsupporting

confidence: 92%

mentioning

confidence: 99%

Formylpeptide Receptor Single Nucleotide Polymorphism 348T>C and Its Relationship to Polymorphonuclear Leukocyte Chemotaxis in Aggressive Periodontitis

Maney

Walters

2009

Journal of Periodontology

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“…Liu et al 40 showed that in two cases of Papillon-Lefevre syndrome, the chemotactic response of polymorphonuclear neutrophils (PMN) to FMLP and to IL-8 was depressed. Sigusch et al 41 observed that chemotactic behaviour of crevicular PMN is altered in localized early onset periodontitis (LEOP) and generalized early onset periodontitis (GEOP) lesions. In the present study, N-FMLP and casein were used as chemotactic agents.…”

Section: Discussionmentioning

confidence: 99%

The investigation of the ultrastructural neutrophil changes in alloxan‐induced diabetes in rats: response to a chemotactic challenge

Özsoy

Bostanci

Ayvalı

2003

Cell Biochemistry & Function

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Experimental diabetes is one of the most popular conditions in which to study the relation between neutrophil leukocyte activity and periodontal destruction. The aetiology of neutrophil dysfunction in the gingival tissue associated with diabetes has yet to be clarified. Diabetes in rats decreases neutrophil chemotactic activity in proportion to the severity of this systemic disorder. The present study was carried out to evaluate the relationship between the severity of diabetes and the neutrophil response to two chemotactic agents, and to correlate the observed neutrophil defects with the degree of diabetes. In this study two chemotactic agents, casein (0.2 microl, 2 mg ml(-1)) or N-formylmethionylleucylphenylalanine (FMLP; 0.2 microl, 10(-4) M), were placed into the gingival crevices of alloxan-induced diabetic rats. Gingival biopsies were taken 15 min later and then at 5-min intervals up to 45 min and investigated by electron microscopy. Adherence and migration were observed in the rats with moderate diabetes 30 min after the application of casein. There was chemotaxis after 35 min of administration of the peptide FMLP. By 40 min neutrophils with pyknotic nuclei were observed. At 45 min neutrophils with a decreased number of granules were present. As the severity of the diabetes increased, the neutrophils degenerated and were structurally distorted. In the rats which had alloxan-induced diabetes there was abnormal periodontal damage. This damage is thought to be related to dysfunctional neutrophils. These findings many contribute to an answer to the following question: why is there an apparent variability in the susceptibility of periodontal breakdown in diabetics?

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“…Thus, synergistic or additive effects are to be expected, but probably also opposing, conflicting signals. Analyzing cells derived from the inflamed sites or from the peripheral blood of patients with systemic inflammatory diseases, including sepsis, gives some insight into the complex alterations of PMN (38)(39)(40)(41)(42)(43)(44)(45)(46).…”

Section: Discussionmentioning

confidence: 99%

Polymorphonuclear Neutrophils in Posttraumatic Osteomyelitis: Cells Recovered From the Inflamed Site Lack Chemotactic Activity but Generate Superoxides

Wagner¹,

Kaksa

Müller

et al. 2004

Shock

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The pathogenesis of posttraumatic osteomyelitis, one of the major complications after orthopedic surgery, is not yet understood. Formation of bacterial biofilms on the implant is presumed, conferring resistance to antibiotic therapy and probably also to the host defense mechanisms. In that context, the polymorphonuclear neutrophils (PMN) having infiltrated the infected site were recovered and characterized phenotypically and functionally. Loss of CD62L and upregulation of CD14 were seen, as was expression of CD83. Expression of the latter is dependent on de novo protein synthesis and thus is indicative of an extended life span and a transdifferentiation of the PMN at the infected site. The infiltrated PMN had lost their chemotactic activity, whereas the capacity to produce superoxides was preserved and in some patients even enhanced. In vitro experiments done in parallel showed that long-term culture with interferon-gamma resulted in similar alterations of PMN: loss of chemotactic activity, whereas other functions of PMN, such generation of superoxides and phagocytosis of opsonized bacteria, were preserved or even enhanced. The loss of the migratory capacity of PMN having already emigrated from the blood vessel to the infected site is not expected to affect the host defense negatively. Assuming, however, that bacteria are organized as a biofilm and that infiltration into this biofilm is required for phagocytosis of the bacteria, our data could to some extent explain why despite being activated, the PMN are not able to control the infection. By releasing their cytotoxic, proteolytic, and collagenolytic potential, PMN might instead contribute to tissue destruction and eventually to osteolysis.

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Altered chemotactic behavior of crevicular PMNs in different forms of periodontitis

Abstract: These results indicate an increase of chemotactic activity from CF-PMN in patients with adult periodontitis, but on the other hand, a significant reduction of chemotactic responsiveness of these cells in LEOP and GEOP lesions.

Cited by 26 publications

References 39 publications

Formylpeptide Receptor Single Nucleotide Polymorphism 348T>C and Its Relationship to Polymorphonuclear Leukocyte Chemotaxis in Aggressive Periodontitis

Formylpeptide Receptor Single Nucleotide Polymorphism 348T>C and Its Relationship to Polymorphonuclear Leukocyte Chemotaxis in Aggressive Periodontitis

The investigation of the ultrastructural neutrophil changes in alloxan‐induced diabetes in rats: response to a chemotactic challenge

Polymorphonuclear Neutrophils in Posttraumatic Osteomyelitis: Cells Recovered From the Inflamed Site Lack Chemotactic Activity but Generate Superoxides

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