No abstract

Neutrophils (PMN) are considered to be key components in the protection of the periodontium against pathogenic bacteria. We therefore compared five of the major characteristics of peripheral blood PMN (PB‐PMN) (adherence, chemotaxis, phagocytosis, oxidaiive metabolism, and lysosomal granules) to those of normal crevicular neutrophils (CR‐PMN) isolated from the same individuals. The data indicate that the presence of Fc and C3b receptors, and the production of superoxide are similar in CR‐PMN and PB‐PMN. In addition, healthy gingival sulci harbor a high percentage of stimulated PMN as determined by the nitroblue tetrazolium (NBT) reduction assay. The percentage of CR‐PMN which phagocytized opsonized red blood cells (RBC) was lower than that of PB‐PMN. The in vitro migration of CR‐PMN was reduced as compared to that of PB‐PMN. Crevicular neutrophils also have a diminished ability to adhere to glass surfaces which may be related to a direct non‐cytotoxic effect of gingival fluid component(s) on CR‐PMN. In addition, morphologic evidence indicates that specific granules are more depleted than azurophil granules in CR‐PMN. Interpretation of studies of neutrophil functions in periodontal diseases must consider the observed differences between normal peripheral blood and crevicular neutrophils.

Neutrophil specific granules are thought to be important in the evolution of the inflammatory response. Specific granules are preferentially released with minor membrane perturbation in vitro or in vivo, and secreted products probably have important effects on humoral and cellular components of inflammation. In vitro studies reveal that some secreted specific granule products activate the complement cascade to generate the chemoattractant C5a and the opsonin C3b, while other secreted products are selectively chemotactic for monocytes. Translocation of receptors for chemoattractants (fmet-leu-phe) and opsonins (C3bi) from specific granules or closely related organelles to the plasma membrane may play an important role in chemotaxis, adherence, and phagocytosis. Similar translocation of constituents of the electron transport chain involved in the respiratory burst (i.e. cytochrome b) probably plays a role in neutrophil oxidative metabolism and hydrogen peroxide generation. In vivo and in vitro studies of neutrophils from patients with congenital specific granule deficiency, acquired specific granule deficiency (thermal injury and neonates), or normal neutrophils experimentally depleted of nuclei and organelles support these conclusions. Thus, release of specific granule constituents appears to be important for amplification of the initial and subsequent phases of the inflammatory response.

Normal volunteers were infected with hookworm larvae Necator americanus. Peripheral blood counts showed a mean of 524 +/- 29 eosinophils/mm3 of blood before infection and a mean of 3,008 +/- 456 eosinophils/mm3 of blood during infection (P less than .01). Absolute numbers of neutrophils did not change. Eosinophils and neutrophils from the infected period were compared with the noninfected state in each subject. The percentage of hypodense eosinophils increased from a mean of 34% +/- 13% to 80% +/- 7% during infection (P less than .05). Superoxide production of eosinophils increased from a mean of 56 +/- 9 to 97 +/- 12 nmol of O2-./10(6) cells per 60 min (P less than .05) during infection. Chemotaxis of eosinophils to Escherichia coli endotoxin-activated serum increased from a mean average distance migrated of 19 +/- 2 micron (P less than .05), whereas neutrophil responsiveness did not change. This is the first report of changes in eosinophil density and stimulation of eosinophil function in normal hosts experimentally infected with hookworm. The data indicate that hookworm infection preferentially increases eosinophil production and activity with little effect on neutrophils.