Augmentation of Human Polymorphonuclear Leukocyte Adherence by Interferon

Thong²,

McCormack³

et al. 1988

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Human neutrophil adherence was enhanced by recombinant human tumour necrosis factor-β (TNF/J) but suppressed by recombinant human interleukin-2 (IL-2). The opposite effects of these two lymphokines were observed over a range of concentrations consistent with their other biological activities, occurred within 15 min of incubation, and were still evident after 60 min. Pretreatment of neutrophils with both IL-2 and TNFβ resulted in adherence values intermediate between the values obtained with the individual lymphokines. IL-2 suppressed the stimulatory effects of both the chemotactic peptide formyl-methionyl-leucyl-phenylalanine (FMLP) and the phorbol ester phorbol myristate acetate (PMA). The combination of TNFβ with either FMLP or PMA produced enhancement of neutrophil adherence which exceeded that of either agent alone. These effects of the lymphokines were not due to endotoxin contamination since their effects were sensitive to heating and insensitive to polymyxin B treatment. These experiments provide further evidence for the critical role of these lymphokines in the regulation of acute and chronic inflammatory processes.

Section: Discussionmentioning

confidence: 99%

Lymphocyte-Neutrophil Interactions: Opposite Effects of Interleukin-2 and Tumour Necrosis Factor-Beta (Lymphotoxin) on Human Neutrophil Adherence

Thong²,

McCormack³

et al. 1988

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“…The PMN adherence assay was performed using nylon fiber microcolumns, as previously described [20,21). Briefly, the nylon fiber microcolumns were prepared by carefully weighing out 10 mg lots of teased nylon fiber (Olympic Products, Queenslane, Aus tralia).…”

Section: Pmn Adherencementioning

confidence: 99%

“…The resultant change in PMN behavior is measured with the adherence mi croassay developed in our laboratory [20,21]. Adher ence is one of the earliest observable and crucial changes in PMN behavior following PMN activation [22].…”

Section: Introductionmentioning

confidence: 99%

Direct Modulation of Human Neutrophil Adherence by Coaggregating Periodontopathic Bacteria

Seymour

Thong

1987

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Direct interaction between Fusobacterium nucleatum and PMNs produced consistent enhancement of PMN adherence. In contrast, consistent suppression of PMN adherence was observed after direct interactions between PMNs and Bacteroides gingivalis or Actinomyces viscosus. The modulatory effects of these periodontopathic bacteria on PMN function could be seen as early as 2 min after interaction. The effects were abrogated by alteration of bacterial structural integrity with heat, formalin or ultrasonic disruption. Carbohydrate or glycoprotein receptors on PMNs may be involved because the effects were blocked by monosaccharides in the medium. Coaggregation experiments showed that permutations involving F. nucleatum always resulted in enhancerrtent of PMN adherence, and that this can be blocked by D-galactose. These findings may have implications in the initiation and sustenance of chronic inflammatory tissue damage in periodontitis.

“…The PMN adherence microassay was performed using nylon fiber microcolumns as previously described [13,18]. Briefly, the nylon fiber microcolumns were prepared by packing 10-mg lots of teased nylon fiber (Olympic Products, Queensland, Australia) into 100-p.l disposable pipette tips (Stockwell Scientific, Calif.) so as to occupy the center 2-cm portion of the 5-cm pipette tip.…”

Section: Pmn Adherencementioning

confidence: 99%

Modulation of Human Neutrophil Adherence by Periodontopathic Bacteria: Reversal by Specific Monoclonal Antibodies

Bird²,

Seymour³

et al. 1989

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Previous investigations by us have shown that direct interaction of Fusobacterium nucleatum with polymorphonuclear neutrophils (PMNs) results in the stimulation of PMN adherence whereas direct interaction with Bacteroides gingivalis results in PMN suppression. In the present study, panels of monoclonal antibodies (MAbs) raised against cell wall antigens of F. nucleatum and B. gingivalis were tested to determine their ability to block the modulatory effects of the bacteria in their interactions with PMNs. While no activity was demonstrated for any of the 9 MAbs raised against F. nucleatum, it was found that 2 of 16 MAbs raised against B. gingivalis were able to reverse the suppression of PMN adherence induced by the bacteria. Further studies on these 2 reactive MAbs showed that the effect of MAbs were abrogated by heat treatment as well as by trypsin proteolysis. Investigations into the nature of the reactive epitopes on the bacterial surface showed that they probably contain protein components susceptible to proteolytic attack by subtilisin. In addition, β-galactose may be a component of the reactive epitopes for one of the MAbs, but sialic acid residues on the bacterial surface are probably not involved as their elimination by neuraminidase did not affect the binding of both MAbs. The results of the present study strongly validate our previous observations that direct specific interaction of B. gingivalis with human PMNs occurs, resulting in the suppression of PMNs.