The effects of live Neisseria meningitidis and tumour necrosis factor‐α on neutrophil oxidative burst and β2‐integrin expression

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Abstract
The effects of human recombinant tumour necrosis factor‐α (TNF‐α) on neutrophil (PMNL) oxidative burst and on CD11b/CD18 and CD14 expression after stimulation with pathogenic or nonpathogenic Neisseria meningitidis were studied using chemiluminescence and flow cytometry. PMNL oxidative burst increased more when stimulated with the apathogenic 29E strain than with the pathogenic B strain both when studied by chemiluminescence and by flow cytometry. When TNF‐α was added to whole blood or PMNL together with bacteria a significant increase in the oxidative burst was seen for the B strain only. When whole blood was preincubated for 30 min with TNF‐α the increase in oxidative burst was significant for both meningococcal strains. TNF‐α caused a significant increase in PMNL CD11b/CD18 expression after 30 min of incubation at 37°C. TNF‐α added simultaneously with the bacteria induced a significant increase in PMNL CD11b/CD18 in both strains. Incubation with the B strain alone caused a low but significant increase in CD11b/CD18 expression, but the addition of TNF‐α increased this expression to the same high level as incubation with TNF‐α alone or the 29E strain alone. Only TNF‐α and the 29E strain caused significant increases in CD14 expression. In conclusion, human PMNLs react differentially when stimulated with pathogenic and nonpathogenic N. meningitidis and the activating effect of TNF‐α is variable depending on the bacteria involved.