l-Arginine Ameliorates Lipopolysaccharide-Induced Intestinal Inflammation through Inhibiting the TLR4/NF-κB and MAPK Pathways and Stimulating β-Defensin Expression in Vivo and in Vitro
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Abstract
<p class="first" id="d14577918e109">Nutritional regulation of endogenous antimicrobial
peptide (AMP) expression is considered
a promising nonantibiotic approach to suppressing intestinal infection of pathogen.
The current study investigated the effects of l-arginine on LPS-induced intestinal
inflammation and barrier dysfunction in vivo and in vitro. The results revealed that
l-arginine attenuated LPS-induced inflammatory response, inhibited the downregulation
of tight junction proteins (TJP) (p < 0.05) by LPS, and maintained intestinal integrity.
In porcine intestinal epithelial cells (IPEC-J2), l-arginine obviously suppressed
(p < 0.05) the levels of IL-6 (220.63 ± 2.82), IL-8 (333.95 ± 3.75), IL-1β (693.08
± 2.38), and TNF-α (258.04 ± 4.14) induced by LPS. Furthermore, l-arginine diminished
the LPS-induced expression of Toll-like receptor 4 (TLR4) and inhibited activation
of TLR4-mediated nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase
(MAPK) signaling pathways. Importantly, we proposed a new mechanism that l-arginine
had the ability to stimulate the expression of porcine epithelial β-defensins through
activating the mammalian target of the rapamycin (mTOR) pathway, which exerts anti-inflammatory
influence. Moreover, pBD-1 gene overexpression decreased (p < 0.05) the TNF-α level
stimulated by LPS in IPEC-J2 cells (4.22 ± 1.64). The present study indicated that
l-arginine enhanced disease resistance through inhibiting the TLR4/NF-κB and MAPK
pathways and partially, possibly through increasing the intestinal β-defensin expression.
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