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-Inducing Factors but Enhances NK Cell Production of IFN-1
,
Departments of
*
Medicine and
Physiology, East Carolina University School of Medicine, Greenville, NC 27858;
Department of Biology, Southern College of SDA, Collegedale, TN 37315;
§
Laboratory of Host Defense, Institute for Advanced Medical Sciences, Hyogo College of Medicine, Nishinomiya, Japan;
¶
Hayashibara Biochemical Laboratories, Okayama, Japan;
||
Japan BCG Laboratory, Tokyo, Japan; and
#
Myrvik Enterprises, Southport, NC 28461
In our study of the immunoregulatory roles of IL-10 in innate
immunity, nonantigenic phagocytosable chitin particles were
administered i.v. to IL-10-deficient (knockout (KO)) mice or KO mice
pretreated with anti-NK1.1 or anti-IFN-
Abs. The results
established that chitin treatment of KO mice increased superoxide anion
release from alveolar macrophages (M
) to a level much higher than
that in wild-type (WT) mice. The results also suggested that the NK
cell is the source of IFN- that is primarily responsible for this
alveolar M priming. To further study the roles of IL-10-inhibiting
chitin-induced IFN- production, we used spleen cell cultures. The
experiments showed that IL-12, IL-18, and TNF-
, which were produced
by chitin-stimulated M, contributed to the IFN--inducing activity
of chitin. Our results established that exogenous IL-10 inhibited
chitin-induced IFN- production in spleen cell cultures from both KO
and WT mice. Exogenous IL-10 also inhibited IL-12 and TNF-
production by chitin-stimulated M. Exogenous IL-10 decreased IL-12-
or IL-18-induced IFN- levels in KO but not in WT NK cell cultures.
However, exogenous IL-10 enhanced IFN- levels when NK cells were
stimulated simultaneously with both IL-12 and IL-18 in KO and WT
cultures. Our in vitro data indicate that IL-10 has differential
effects on chitin-induced IFN- production. However, the inhibitory
effects of endogenous IL-10 appear to be dominant in the chitin-induced
alveolar M priming response in vivo.
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