The response of human sulcular leucocytes to a chemotactic challenge

Golub, Lorne M.; Iacono, Vincent J.; Nicoll, Gregg A.; Ramamurthy, N.; Kaslick, Ralph S.

doi:10.1111/j.1600-0765.1981.tb00963.x

Cited by 31 publications

(21 citation statements)

References 38 publications

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“…Hill et al (J977) have reported that a transient increase in PMN chemotactic responsiveness may be associated with bacterial infection. Using an in vivo chemotactic assay with casein as the attractant, Golub et al (1981) and Singh et al (1982) have shown that the influx of crevicular PMNs was greater in patients with juvenile periodontitis than controls. Using an in vivo chemotactic assay with casein as the attractant, Golub et al (1981) and Singh et al (1982) have shown that the influx of crevicular PMNs was greater in patients with juvenile periodontitis than controls.…”

Section: Discussionmentioning

confidence: 99%

Neutrophil chemotactic behaviour in patients with early‐onset forms of periodontitis

Kinane

Cullen

Johnston

et al. 1989

J Clinic Periodontology

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Despite some reports to the contrary, it is generally assumed that early-onset forms of periodontal disease (including both juvenile and rapidly progressive periodontitis) are associated with a defect in neutrophil (PMN) chemotactic behaviour. Using the Boyden chamber technique and N-formyl-methionyl-leucylphenylalanine (FMLP) to assess locomotion by the leading front method, we have failed to show any evidence for such depressed PMN locomotion. Indeed, when PMN chemotaxis and chemokinesis are considered in response to a range of chemoattractant doses our results indicate significant enhancement of all but random locomotion. When taken together with other studies, our results suggest that PMNs from patients with early-onset periodontitis may show abnormal locomotory behaviour which can either be enhanced or reduced in nature. The extent to which these results reflect in vitro methodology in uncertain and, furthermore, their in vivo significance is unclear.

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Section: Discussionmentioning

confidence: 99%

Neutrophil chemotactic behaviour in patients with early‐onset forms of periodontitis

Kinane

Cullen

Johnston

et al. 1989

J Clinic Periodontology

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“…This histological evidence unequivocally demonstrated an increase in polymorphonuclear leukocyte emigration into the gingiva as the first histological indication of a gingival inflammatory response. As later demonstrated by Klinkhamer and Zimmerman (1969) and later by Golub et al (1981), this response can occur within minutes to hours, rather than the days to weeks it normally takes to identify the clinical signs.…”

Section: Short-chain Carboxylic Acid Generation By Periodontal Microbmentioning

confidence: 93%

“…The effects are dose-and acid-dependent in the mM range, with butyric > propionic > acetic > lactic acid. In addition, SCCA were found to inhibit periodontal ligament fibroblast adhesion (Eftimiadi et al, 1993 (Klinkhamer and Zimmerman, 1969;Golub et al, 1981) or SCCA . Normal neutrophil apoptosis is prevented by stimulation with a number of chemoattractants, cytokines, and butyrate (for review, see Liles and Klebanoff, 1995;Savill and Haslett, 1995;Stringer et al, 1996).…”

Section: Epithelium and Endotheliummentioning

confidence: 99%

Short-Chain Carboxylic-Acid-Stimulated, PMN-Mediated Gingival Inflammation

Niederman

Zhang²,

Kashket³

1997

Critical Reviews in Oral Biology & Medicine

118

104

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This communication reviews the effects of short-chain carboxylic acids on human cells of importance to the periodontium. The central hypothesis is that these acids can alter both cell function and gene expression, and thus contribute to the initiation and prolongation of gingival inflammation.Short-chain carboxylic acids [CH3-(CH2)x-COOH, x < 31 are metabolic intermediates with a broad range of apparently paradoxical biological effects. For example, lactic acid (CH3-CHOH-COOH), a 3-carbon alpha-hydroxy-substituted acid, is widely recognized for its cariogenicity. Lactic acid, however, also occurs in tropical fruits, and is the active ingredient in a variety of anti-wrinkle creams developed by dermatologists. In marked contrast, the unsubstituted 3-carbon propionic acid (CH3-CH2-COOH) is used as a food preservative and is the active principle for one class of non-steroidal anti-inflammatory agents. Interestingly, the addition of one carbon to propionic acid dramatically changes the biological effects. The unsubstituted 4-carbon butyric acid (CH3-CH2-CH 2-COOH) is used by hematologists as a de-differentiating agent for the treatment of sickle cell anemia, but by oncologists as a differentiating agent for cancer chemotherapy. Finally, acting either individually or in concert, these acids can increase vascular dilation. Clearly, these acids, while metabolically derived, have a number of very divergent activities which are cell-type-specific (Fig. 1).It may be telling that periodontal bacteria produce these acids in millimolar concentrations, and that these bacteria can be characterized by their acid production profiles. It is no less interesting that these acids occur in the gingival crevices of human subjects with severe periodontal disease at millimolar levels which are > 10-fold higher than those found in mildly diseased subjects, and are undetectable in healthy subjects. Further, when applied directly to healthy human gingiva, short-chain carboxylic acids stimulate a gingival inflammatory response and inflammatory cytokine release, At the cellular level, these acids inhibit proliferation of gingival epithelial and endothelial cells, and inhibit leukocyte apoptosis and function, but can stimulate leukocyte cytokine release. At the molecular level, these acids can stimulate neutrophil gene transcription, translation, and protein expression. Thus, the likelihood is high that these acids, in addition to their cariogenic activity, can promote and prolong gingival inflammation.Our challenge will be to identify the cell or cells of the periodontium which respond to short-chain carboxylic acids, to delineate their responses and the molecular mechanism(s) of these effects, and to categorize the aspects of the inflammatory components which damage and those which protect the host. With this information, it may be possible to begin to rationally identify and test pharmaceutical agents which diminish the harmful aspects, while enhancing the beneficial components, of the inflammatory response.

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“…A method of testing the PMN response in the gingival crevice was introduced by Golub, but it exposes cells to mechanical stress. Manual and optical counts have further disadvantages.…”

Section: Discussionmentioning

confidence: 99%

Refractory neutrophil activation in type 2 diabetics with chronic periodontitis

Herrmann

Sonnenschein

Groeger

et al. 2020

J of Periodontal Research

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Background Inflammation increases diabetes mellitus type 2 (T2DM) progression and severity. T2DM patients are at high risk of the rapid development of chronic periodontitis (CP). Topical presence, high numbers, and bactericidal effects of immune cells are challenged by augmented antigen‐induced inflammation, which promotes both diseases. Objectives To investigate gingival cellular inflammatory responses in individuals with previously undiagnosed T2DM with CP or CP alone and in systemically and periodontally healthy controls (H) in vivo and to establish an ex vivo technique permitting quantitative and qualitative assessments of gingival crevicular immune cells. Materials and Methods T2DM + CP, CP, and H individuals (n = 10, each) received a 2‐week oral hygiene regimen (OHR). Afterwards, a noninvasive sampling technique was performed to evaluate gingival inflammation induced under standardized conditions in vivo, that is, in the absence of severe periodontal destruction and inflammation at clinically healthy sites. Stimuli (casein/test or phosphate‐buffered saline w/o. Ca2+ or Mg2+, PBS(−/−)/control) were randomly applied contralaterally in the gingival sulci of participants’ upper dentes canini. One day after completion of the OHR, gingival crevicular fluid (GCF) was kinetically assayed between the time of the baseline (BL) measurement and 55 minutes. Polymorphonuclear leukocyte (PMN) content (PMNGCF) was quantitated at an optimum time of 35 minutes. PMNGCF counts reflect local inflammation. Ex vivo samples were fluorimetrically labeled, gated according to the donor's peripheral blood polymorphonuclear neutrophils (PMNPB), and then counted, employing flow cytometry. Results PMNGCF counts in unstimulated gingival crevices (at BL) in the T2DM + CP group were higher than those in the CP and H groups. PMNGCF counts were elevated in casein vs PBS(−/−)‐stimulated gingival crevices in all groups. Patients with T2DM + CP showed increased PMNGCF counts compared to those with CP (P = .035) according to scatter plots. CD45+ counts in the stimulated sites in T2DM + CP patients were higher than those in CP and H patients (P = .041). Under stimulation conditions, the CD45+ counts differed from those under placebo conditions (P = .019), indicating augmented, inducible inflammatory leukocyte infiltrate in T2DM + CP patients. Conclusions This noninvasive technique permits quantitative assessment of (experimental) gingival inflammation in vivo, revealing an influence of T2DM + CP on the number of primary immune cells in the gingival crevice. Patients who are challenged with (local) leukocytosis are likely at risk of collateral damage to the gingival crevice neighboring tissues, favoring the severity and progression of CP and consequently T2DM (http://www.clinicaltrials.gov NCT01848379).

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The response of human sulcular leucocytes to a chemotactic challenge

Cited by 31 publications

References 38 publications

Neutrophil chemotactic behaviour in patients with early‐onset forms of periodontitis

Neutrophil chemotactic behaviour in patients with early‐onset forms of periodontitis

Short-Chain Carboxylic-Acid-Stimulated, PMN-Mediated Gingival Inflammation

Refractory neutrophil activation in type 2 diabetics with chronic periodontitis

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