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B Pathway and Exploits Lipopolysaccharide Signaling to Trigger Apoptosis in Macrophages1
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Max von Pettenkofer-Institut für Hygiene und Medizinische Mikrobiologie, München, Germany; and
Institut National de la Santé et de la Recherche Médicale Unité 431, Université Montpellier II, Montpellier, France
Exposure of macrophages to bacteria or LPS mediates activation of
signaling pathways that induce expression of self defense-related
genes. Pathogenic Yersinia species impair activation of
transcription factor NF-
B and trigger apoptosis in macrophages. In
this study, we dissected the mechanism of apoptosis induction by
Yersinia. Selectively, Yersinia
enterocolitica strains producing the effector protein
Yersinia outer protein P (YopP) hampered NF-B
activation and subsequently conferred apoptosis to J774A.1 macrophages.
Thereby, YopP bound and inhibited the macrophage NF-B-activating
kinase IKK
. YopP- and Yersinia-, but not
Salmonella-induced apoptosis was specifically prevented
by transient overexpression of NF-B p65, giving evidence that YopP
mediates cell death by disrupting the NF-B signaling pathway.
Transfection of J774A.1 macrophages with YopP induced a moderate, but
significant degree of apoptosis (40–50% of transfected cells). This
effect was strongly enhanced by additional initiation of LPS signaling
(80–90%), indicating a synergism between LPS-induced signal
transduction and inhibition of NF-B by YopP. This reflects a
strategy of a bacterial pathogen that takes advantage of LPS, serving
as cofactor, to impair the macrophage.
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