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*
Istituto di Microbiologia, Facoltà di Medicina e Chirurgia, Università degli Studi di Messina, Messina, Italy; and
Institute for Cancer Research, University of Trondheim, Trondheim, Norway
Proinflammatory cytokines have an important pathophysiologic role
in septic shock. CD14 is involved in cytokine responses to a number of
purified bacterial products, including LPS. However, little is known of
monocyte receptors involved in cytokine responses to whole bacteria. To
identify these receptors, human monocytes were pretreated with
different mAbs and TNF-
was measured in culture supernatants after
stimulation with whole heat-killed bacteria. Human serum and
anti-CD14 Abs significantly increased and decreased, respectively,
TNF- responses to the Gram-negative Escherichia coli.
However, neither treatment influenced responses to any of the
Gram-positive bacteria tested, including group A and B streptococci,
Listeria monocytogenes, and Staphylococcus
aureus. Complement receptor type III (CR3 or CD18/CD11b) Abs
prevented TNF- release induced by heat-killed group A or B
streptococci. In contrast, the same Abs had no effects when monocytes
were stimulated with L. monocytogenes or S.
aureus. Using either of the latter bacteria, significant
inhibition of TNF- release was produced by Abs to CD11c, one of the
subunits of CR4. To confirm these blocking Ab data, IL-6 release was
measured in CR3-, CR4-, or CD14-transfected Chinese hamster ovary cells
after bacterial stimulation. Accordingly, streptococci triggered
moderate IL-6 production (p < 0.05) in CR3 but not
CD14 or CR4 transfectants. In contrast, L. monocytogenes
and S. aureus induced IL-6 release in CR4 but not CR3 or
CD14 transfectants. Collectively our data indicate that
ß2 integrins, such as CR3 and CR4, may be involved in
cytokine responses to Gram-positive bacteria. Moreover, CD14 may play a
more important role in responses to whole Gram-negative bacteria
relative to Gram-positive ones.
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