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DOI 10.1046/j.1469-0691.2001.00216.x

Медицинская библиотека · Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases · 2001

The effects of live Streptococcus pneumoniae and tumor necrosis factor-alpha on neutrophil oxidative burst and beta 2-integrin expression.

Kragsbjerg P, Fredlund H

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Аннотация

OBJECTIVE

To study the effects of TNF-alpha and live Streptococcus pneumoniae on human neutrophil oxidative burst and beta 2-integrin expression using flow cytometry.

METHODS

Six clinical isolates of S. pneumoniae (serotypes 3, 19A, 22F, 6A, 33F and 9N) from patients with bacteremic pneumonia or upper respiratory tract infections were studied. Whole blood was incubated either alone, with TNF-alpha or with S. pneumoniae or with both TNF-alpha and pneumococci at a ratio of one neutrophil per 1--5 bacteria. After 30 min of incubation, the tubes were put into ice, fixed and analysed.

RESULTS

S. pneumoniae caused an increase in oxidative burst but not greater than that caused by TNF-alpha alone. When whole blood was preincubated with TNF-alpha for 30 min before the addition of pneumococci, a further increase in the oxidative burst response was seen. The variation in CD11b expression was not significant. Both S. pneumoniae and TNF-alpha caused increases in CD18 expression. The addition of TNF-alpha directly with the bacteria caused no further increase, but preincubation of blood with TNF-alpha 30 min before the addition of the bacteria caused a significant increase in CD18 expression.

CONCLUSIONS

Live S. pneumoniae stimulates polymorphonuclear leukocytes to produce an oxidative burst and increases expression of CD18, and these effects are enhanced by TNF-alpha.

Для цитирования: Kragsbjerg P, Fredlund H. The effects of live Streptococcus pneumoniae and tumor necrosis factor-alpha on neutrophil oxidative burst and beta 2-integrin expression.. Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases. 2001. DOI: 10.1046/j.1469-0691.2001.00216.x.

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