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* Max von Pettenkofer-Institut für Hygiene und Medizinische Mikrobiologie, Ludwig-Maximilians-Universität München, D-80336 München, Germany;
Medizinische Poliklinik, Ludwig-Maximilians-Universität München, D-80336 München, Germany; and
Klinik für Dermatologie und Allergologie, Ludwig-Maximilians-Universität München, D-80337 München
3Correspondence: Max von Pettenkofer-Institut, Ludwig-Maximilians-Universität München, Pettenkoferstrasse 9a, D-80336 München, Germany. E-mail: Autenrieth{at}m3401.mpk.med.uni-muenchen.de
Enteropathogenic Yersinia bacteria trigger the production of the
proinflammatory chemokine IL-8, an important chemokine for the
recruitment of polymorphonuclear leukocytes (PMN).
Yersinia is resistant to phagocytosis by PMN, and the
recruitment of these cells is thought to be part of a pathogenic
strategy of Yersinia to establish infection by allowing
the pathogen to gain access to, and disseminate within, host tissue. We
report here that Yersinia expressing the outer membrane
protein invasin triggers IL-8 production in epithelial cells. The 195
carboxyl-terminal amino acids of invasin when linked to latex beads are
sufficient to trigger IL-8 production. By means of IL-8 promoter
reporter gene assays and electrophoretic mobility shift assay
experiments, the minimal optimal region of the IL-8 promoter responsive
to invasin was identified and invasin-responsive control elements were
characterized. Invasin-induced activation of the IL-8 promoter was
found to be mediated through a previously identified NF-
B element.
This NF-B binding site preferentially binds Rel p65-p65 homodimers
as well as some p50-p65 heterodimers in response to stimulation by
invasin. Invasin-induced NF-B activation correlated with degradation
of IB
and the inhibition of NF-B by specific inhibitors of
IB activation blocked invasin-induced IL-8 secretion.
Invasin-triggered IL-8 production does not depend on invasin-triggered
uptake of bacteria, and is independent of a functional PI3-kinase. This
report is the first to demonstrate the molecular basis of IL-8
production triggered by enteropathogenic bacteria. Together, these data
elucidate the possible early pathomechanisms operating in
Yersinia infection and may have implications for the
design of novel therapeutics directed against this
enteropathogen.—Schulte, R., Grassl, G. A., Preger, S., Fessele,
S., Jacobi, C. A., Schaller, M., Nelson, P. J., Autenrieth,
I. B. Yersinia enterocolitica invasin protein
triggers IL-8 production in epithelial cells via activation of Rel
p65-p65 homodimers.
Key Words: bacteria • chemokine • transcription • NF-B
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