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Infection and Immunity, June 2000, p. 3581-3586, Vol. 68, No. 6
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Gram-Positive Bacteria Are Potent Inducers of
Monocytic Interleukin-12 (IL-12) while Gram-Negative Bacteria
Preferentially Stimulate IL-10 Production
Christina
Hessle,*
Bengt
Andersson, and
Agnes E.
Wold
Department of Clinical Immunology,
Göteborg University, SE-413 46 Göteborg, Sweden
Received 29 November 1999/Returned for modification 3 February
2000/Accepted 22 March 2000
Interleukin-10 (IL-10) and IL-12 are two cytokines secreted by
monocytes/macrophages in response to bacterial products which have
largely opposite effects on the immune system. IL-12 activates cytotoxicity and gamma interferon (IFN-
) secretion by T cells and NK
cells, whereas IL-10 inhibits these functions. In the present study,
the capacities of gram-positive and gram-negative bacteria to induce
IL-10 and IL-12 were compared. Monocytes from blood donors were
stimulated with UV-killed bacteria from each of seven gram-positive and
seven gram-negative bacterial species representing both aerobic and
anaerobic commensals and pathogens. Gram-positive bacteria induced much
more IL-12 than did gram-negative bacteria (median, 3,500 versus 120 pg/ml at an optimal dose of 25 bacteria/cell; P < 0.001), whereas gram-negative bacteria preferentially stimulated secretion of IL-10 (650 versus 200 pg/ml; P < 0.001). Gram-positive species also induced stronger major
histocompatibility complex class II-restricted IFN-
production in
unfractionated blood mononuclear cells than did gram-negative species
(12,000 versus 3,600 pg/ml; P < 0.001). The
poor IL-12-inducing capacity of gram-negative bacteria was not
remediated by addition of blocking anti-IL-10 antibodies to the
cultures. No isolated bacterial component could be identified that
mimicked the potent induction of IL-12 by whole gram-positive bacteria,
whereas purified LPS induced IL-10. The results suggest that
gram-positive bacteria induce a cytokine pattern that promotes Th1
effector functions.
*
Corresponding author. Mailing address: Department of
Clinical Immunology, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden. Phone: 46-31-342 41 73. Fax:
46-31-342 46 21. E-mail:
christina.hessle{at}immuno.gu.se.
Infection and Immunity, June 2000, p. 3581-3586, Vol. 68, No. 6
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
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