Chlamydia pneumoniae infection suppresses Staphylococcus enterotoxin B-induced proliferation associated with down-expression of CD25 in lymphocytes

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Abstract:

Chlamydia pneumoniae (Chlamydophila pneumoniae) infects lymphocytes and modulates their immune functions; this is critical in the development of chronic inflammatory diseases associated with this pathogen. Therefore, to clarify this immune modulation due to C. pneumoniae infection, the effect of this infection on the proliferation of human peripheral blood lymphocytes was examined. Lymphocytes were proliferated by stimulation with Staphylococcus aureus enterotoxin B, and the cell number was increased up to 3 times the unstimulated lymphocyte number. Further, induction of CD25 expression was observed in 55.8% of lymphocytes. Infection with C. pneumoniae suppressed the proliferation of almost half the lymphocytes induced by stimulation with S. aureus enterotoxin B, and CD25 induction was inhibited in 64.7% of lymphocytes. Inhibition of CD25 expression was observed in both infected and uninfected lymphocytes in culture. However, the expression of VLA4 was not affected by C. pneumoniae infection. Furthermore, inhibition was observed only by infection with viable C. pneumoniae and not by the heat-killed bacteria. These results suggest that C. pneumoniae affects lymphocyte function by inhibiting proliferation and CD25 expression in response to immunological stimulation, possibly via humoral mediator(s).

Chlamydia pneumoniae (Chlamydophila pneumoniae) infecte les lymphocytes et module leurs fonctions immunitaires, ce qui est crucial au développement de maladies inflammatoires chroniques associées à ce pathogène. En conséquence, afin de clarifier les mécanismes responsables de cette modulation immunitaire causée par l’infection à C. pneumoniae, l’effet de cette infection sur la prolifération des lymphocytes du sang périphérique a été examiné. Les lymphocytes ont été stimulés par l’entérotoxine B de Staphylococcus aureus. Le nombre de cellules a presque triplé, comparativement aux lymphocytes non stimulés. De même, une induction du CD25 a été observée chez 55,8 % des lymphocytes. L’infection à C. pneumoniae a supprimé la prolifération de presque la moitié des lymphocytes stimulés par l’entérotoxine B de S. aureus, et l’induction du CD25 a été inhibée chez 64,7 % des lymphocytes. L’inhibition de l’expression de CD25 a été observée tant chez les lymphocytes en culture infectés que non infectés. Cependant l’expression de VLA4 n’était pas affectée par l’infection à C. pneumoniae. De plus, l’inhibition n’était observée que lors d’une infection avec C. pneumoniae viable seulement, et non avec les bactéries inactivées par la chaleur. Ces résultats suggèrent que C. pneumoniae affecte la fonction des lymphocytes en inhibant leur prolifération et l’expression de CD25 en réponse à une stimulation immune, probablement par l’intermédiaire de médiateurs humoraux.

Document Type: Research Article

Publication date: April 1, 2010

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  • Published since 1954, this monthly journal contains new research in the field of microbiology including applied microbiology and biotechnology; microbial structure and function; fungi and other eucaryotic protists; infection and immunity; microbial ecology; physiology, metabolism and enzymology; and virology, genetics, and molecular biology. It also publishes review articles and notes on an occasional basis, contributed by recognized scientists worldwide.
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