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Blood, 15 February 2001, Vol. 97, No. 4, pp. 1035-1042
IMMUNOBIOLOGY
Interleukin 9 promotes influx and local maturation of
eosinophils
Jamila Louahed,
Yuhong Zhou,
W. Lee Maloy,
Pyapalli U. Rani,
Christine Weiss,
Yaniv Tomer,
Anne Vink,
Jean-Christophe Renauld,
Jacques Van Snick,
Nicholas C. Nicolaides,
Roy C. Levitt, and
Angela Haczku
From the Magainin Institute of Molecular
Medicine, Magainin Pharmaceuticals, Inc, Plymouth Meeting, PA; Ludwig
Institute for Cancer Research, Brussels Branch, and the Experimental
Medicine Unit, University of Louvain, Brussels, Belgium.
The interleukin 9 (IL-9) pathway has recently been associated
with the asthmatic phenotype including an eosinophilic tissue inflammation. The mechanism by which IL-9 affects eosinophils (eos) is
not known. To investigate whether this cytokine has a direct activity
on the development of eos and eosinophilic inflammation, a model of
thioglycolate-induced peritoneal inflammation was used in IL-9
transgenic (TG5) and background strain (FVB) mice. In this model, a
transient eosinophilic infiltration in the peritoneal cavity was
observed in FVB mice 12 to 24 hours after thioglycolate injection that
coincided with peak IL-5 and IL-9 release. In contrast, TG5 mice
developed a massive eosinophilia that persisted at high levels (81% of
total cells) even 72 hours after thioglycolate injection. Release of
eosinophilic major basic protein (MBP), IL-4, and IL-5 to the
peritoneal cavity of these mice was significantly increased when
compared with the control FVB strain. To study the mechanism by which
IL-9 exerts its effect on eos, bone marrow or peritoneal cells were
cultured in the presence of IL-5, IL-9, or their combination in
vitro. IL-5 alone was able to generate significant numbers of eos in
TG5 but not FVB mice, whereas a combination of IL-5 and IL-9 induced
marked eosinophilia in both strains indicating a synergism between
these 2 cytokines. These data suggest that IL-9 may promote and sustain
eosinophilic inflammation via IL-5-driven eos maturation of precursors.
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