Motility and Adhesiveness in Human Neutrophils

Smith, C. W.; Hollers, James C.; Patrick, Richard A.; Hassett, Clare

doi:10.1172/jci109293

Cited by 220 publications

(43 citation statements)

References 26 publications

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“…Thirdly, contamination, e.g., by viruses (24) or mycoplasma (25), has been shown to alter cell surface properties with respect to interacting cells. To avoid a further misunderstanding, a distinction must be made between "low affinity adhesion," a prerequisite for phagocyte movement on plain surfaces (26), and "high affinity adhesion," that is, the type of (hyper-) adhesion described in the present study which is related to the termination of locomotion of a highly reactive cell (10)(11)(12)(13). While such a distinction is easily made in theoretical terms, it may be difficult to define on practical grounds.…”

Section: Discussionmentioning

confidence: 97%

Antiadhesive properties of biological surfaces are protective against stimulated granulocytes.

Fehr¹,

Moser²,

Leppert³

et al. 1985

J. Clin. Invest.

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When tested on endothelial cell-derived extracellular matrices, neutrophils again showed functional nonresponsiveness to Nformnyl-Met-Leu-Phe. Scanning electron microscopy revealed an impressive congruency between the degree of cellular spreading and metabolic activation iu the presence of N-formylMet-Leu-Phe, with maximally flattened neutrophils on plastic vs. nonspread, polarized cells on monolayers. Identical results were obtained by using other adhesion inducers such as complement-activated plasma or endotoxin. Lack of cell injury by N-formyl-Met-Leu-Phe-exposed neutrophils was corroborated by the absence of tracer release from 1l"njtropolonate-labeled endothelium. These results indicate that biologic surfaces possess antiadhesive properties that protect them from cytotoxic damage by stimulated angry phagocytes.

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Section: Discussionmentioning

confidence: 97%

Antiadhesive properties of biological surfaces are protective against stimulated granulocytes.

Fehr¹,

Moser²,

Leppert³

et al. 1985

J. Clin. Invest.

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“…Many in vitro studies have detailed changes in the state of activation and function of normal PMN in response to inflammatory and infectious stimuli (1,2). What happens to PMN in patients with acute bacterial infections is less clear.…”

Section: Introductionmentioning

confidence: 99%

Studies on phagocytosis in patients with acute bacterial infections.

Simms¹,

Frank

Quinn

et al. 1989

J. Clin. Invest.

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Polymorphonuclear leukocytes (PMN) and monocytes from 20 patients with acute bacterial infections were examined for phagocytic function. PMN of patients expressed markedly enhanced phagocytosis as measured by the ingestion of erythrocyte (E)IgG and IgG/C3b-coated E. Phagocytosis of E coated with C3b alone was not seen, while low levels of ingestion of iC3b-E by patients' PMNs was noted. Monocytes from patients and controls expressed similar phagocytic activity in a fixed endpoint assay; however, the kinetics of phagocytosis by patients' monocytes was strikingly faster. Superoxide anion (02) and myeloperoxidase activities were similar to controls in PMN of four patients studied on day 1 of admission.PMN from two of three patients studied longitudinally showed an initial elevation in EIgG phagocytosis, which fell to normal levels by day 4, concomitantly with increased 0°gener-ation and clinical improvement. Phagocytosis remained elevated in the third patient who did not clear his septicemia.

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“…The mechanism of chemotactic deactivation of human neutrophils has not been elucidated and may vary for different chemotactic factors because the ratio of the optimal deactivating concentration to the maximal chemotactic concentration is a distinct property of each factor. The results of dose-response studies demonstrated that optimal increases in neutrophil adherence and maximal chemotactic deactivation were achieved by the same high concentrations of some chemotactic factors (23,24). However, it could not be established that the increased adherence of the neutrophils induced by the chemotactic factors was directly inhibiting neutrophil chemotaxis, because the concentrations ofthe stimuli that were used concomitantly suppressed random migration and stimulated both hexose-monophosphate shunt activity and lysosomal enzyme release (24).…”

Section: Identification Of Inhibitors Of Chemotaxis and Enhancers Of mentioning

confidence: 99%

“…Thus, as small a quantity as 6 pniol of NAF I or 9 pmol ofNAF II is capable of inhibiting chemotaxis to a maximal extent. In contrast, the maximal chemotactic inhibitory effects of lysozyme and the cationic proteins were achieved with quantities of 30-35 pmol and [20][21][22][23][24][25][26][27][28][29][30] pmol, respectively. Thus, the potency of the NAF as chemotactic inhibitors is at least three to five times that ofthe previously described endogenous inhibitors of neutrophil chemotaxis.…”

Section: Identification Of Inhibitors Of Chemotaxis and Enhancers Of mentioning

confidence: 99%

“…The capacity of diverse chemotactic factors to increase the adherence of human neutrophils to surfaces in vitro has been correlated with the reduced chemotactic responses of comparably treated neutrophils (23,24). The preincubation of neutrophils with most types of chemotactic factors induces a state of unresponsiveness to chemotactic stimulation that is termed chemotactic deactivation (25,26).…”

Section: Identification Of Inhibitors Of Chemotaxis and Enhancers Of mentioning

confidence: 99%

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