DISCUSSIONExperiments 1 and 2 demon

DISCUSSION
Experiments 1 and 2 demonstrate that ADG is improved
by 50 ppm of β-glucan. The improvement in
ADG with β-glucan supplementation (Exp. 2) agrees
with the results reported by Dritz et al. (1995) and
Schoenherr et al. (1994). Dritz et al. (1995) observed
that 250 ppm of β-glucan in nursery-pig diets increased
growth performance but had no effect on G:F. Schoenherr
et al. (1994) concluded that the optimal inclusion concentration of β-glucan was between 250 and 500
ppm when fed throughout the nursery period. Hiss and
Sauerwein (2003) reported that ADFI was increased
when 300 ppm of β-glucan was added to the diet.
The optimal concentration of β-glucan to improve
growth in our study was much less than previously
reported. A possible explanation for this divergence is
the difference in purity, molecular weight, conformation, and extraction methods. Insufficient removal of
protein from β-glucan isolated from yeast cells could
cause a reduction in β-glucan efficacy. Protein can bind
the active terminal residues of β-glucan, thereby preventing
β-glucan from interacting with its receptors
(our unpublished data). In addition, studies on structure-
function relationships of β-glucan using murine
systems have revealed that molecular weight, conformation, and degree of branching affect the binding of
β-glucan with its receptors and therefore influence its
activities (Ohno et al., 1986a,b, 1992).
The exact mechanism through which β-glucan supplementation
improves pig growth performance is unclear.
To the best of our knowledge, no studies have
been conducted to explore the potential of β-glucan to
modulate the production of cytokines, especially antiinflammatory
cytokines. In Exp. 3, diets supplemented
with 50 ppm of β-glucan partially suppressed increases
in plasma concentrations of TNF-α and IL-6 and enhanced
the increase in plasma concentrations of IL-10
brought about by an LPS challenge. It is well known
that IL-6 and TNF-α are proinflammatory cytokines
that not only modulate immunity but also can directly
regulate nutrient metabolism and cause detrimental
effects on animal performance (Spurlock, 1997). The
antiinflammatory cytokine IL-10 (Enk and Katz, 1992)
can inhibit T-cell proliferation, development, and function
(Fuirebtubi et al., 1989) as well as the secretion of
Th1- and Th2-type cytokines (Fuirebtubi et al., 1989;
De Waal Malegyt et al., 1991). Furthermore, IL-10 can
also suppress the activity of the signal transduction
of nuclear transcription factor κB, which is a major
transcription factor of proinflammatory cytokines
(Clarke et al., 1998; Schottelius et al., 1999). If feeding
β-glucan promotes secretion of antiinflammatory cytokines,
such as IL-10, and decreases secretion of proinflammatory
cytokines, such as TNF-α and IL-6, then
less activation of the immune system during the feeding
period would be achieved, which could result in increased
growth performance. This hypothesis is partially
supported by data of Exp. 2 and 3. In Exp. 2, pigs
fed diets supplemented with 50 ppm of β-glucan tended
to have attenuated lymphocyte proliferation on d 14,
indicating that cellular immunity may be suppressed.
In Exp. 3, supplementing pigs with 50 ppm of β-glucan
resulted in a partially suppressed increase in TNF-α
and IL-6 production and enhanced increase in IL-10
production after an LPS challenge. This may help to
explain the increased growth performance observed in
Exp.1 and 2 and in other studies.
Proinflammatory cytokines, such as IL-6 and TNF-
α, are not only primarily associated with immune system,
but also have the potential to alter many aspects
of neuroendocrine function, including the somatotropic
axis (Mandrup-Poulsen et al., 1995; Maule and Vanderkooi,
1999). In the current study, the proinflammatory
cytokine responses of pigs to an LPS challenge were
altered by β-glucan supplementation. Therefore, we further
investigated the influence of β-glucan on somatotropic
response in LPS-challenged pigs. In the current
study, a tendency of mitigating the reduction of plasma
IGF-I was observed in pigs supplemented with β-glucan
after an LPS challenge. Hasselgren (1993) proposed
that the reductions of plasma IGF-I may indicate the
repartition of nutrients away from normal growth and
toward immune response. Other studies also indicated
that plasma IGF-I concentration is associated with pig performance (Prickett et al., 1992; Hathaway et al.,
1993; Hathaway et al., 1996). In our study, although
not significantly different, the tendency of mitigating
the reduction of plasma IGF-I may be an indication that
β-glucan supplementation alleviates the alterations in
somatotropic axis after an LPS challenge, which might
have been associated with the improved performance
in pigs supplemented with β-glucan compared with control
pigs.
Additionally, one of the most interesting observations
from our study was that pigs supplemented with 100
and 200 ppm of β-glucan had lower ADG than pigs
supplemented with 50 ppm of β-glucan. Poutsiaka et
al. (1993) observed that stimulation of human macrophages,
in vitro, with β-glucan resulted in increased
synthesis of IL-1 receptor antagonist, whereas proinflammatory
IL-1β was not increased unless very high
β-glucan doses were applied. Increased concentrations
of IL-1 have been associated with decreased feed intake
and growth performance (Klasing et al., 1987; Blecha
et al., 1995). If feeding β-glucan alters the balance of
IL-1 and IL-1 receptor antagonists such that IL-1 is
preferentially secreted, immune system activation will
increase, potentially resulting in decreased growth performance.
Additionally, Hoffman et al. (1993) demonstrated
that β-glucan at selective doses can either induce
or suppress the release of TNF-α from mononuclear
phagocytes. Therefore, it is possible that diets
supplemented with 100 and 200 ppm of β-glucan in the
current study promoted the secretion of proinflammatory
cytokines such as IL-1, IL-6, and TNF-α instead of
decreasing secretion. This could explain the decreased
growth performance for pigs fed diets supplemented
with 100 and 200 ppm of β-glucan compared with pigs
fed diets supplemented with 50 ppm of β-glucan.