Reticuloendotheliosis virus (REV), a gammaretrovirus in the Retroviridae family, causes an immunosuppressive, oncogenic, and runting-
stunting syndrome in multiple avian hosts.
Allicin, the main effective component of garlic, has a broad spectrum of pharmacological properties. The hypothesis that
allicin could relieve REV-induced immune dysfunction was investigated in vivo and in vitro in the present study. The results showed that dietary
allicin supplementation ameliorated REV-induced dysplasia and immune dysfunction in REV-infected chickens. Compared with the control groups, REV
infection promoted the expression of inflammatory
cytokines including
interleukin (IL)-1β,
IL-6,
IL-10,
interferon (IFN)-γ, and
tumor necrosis factor-α (TNF-α), whereas,
allicin reversed these changes induced by REV
infection. The decreased levels of IFN-α, IFN-β, and
IL-2 were observed in REV-infected chickens, which were significantly improved by
allicin.
Allicin suppressed the REV-induced high expression of
toll-like receptors (TLRs) as well as
melanoma differentiation-associated gene 5 (MDA5) and the activation of
mitogen-activated protein kinase (MAPK) and the
nuclear factor kappa B p65. REV stimulated the phosphorylation of JNK, ERK, and p38, the downstream key signaling molecules of MAPK pathway, while
allicin retarded the augmented phosphorylation level induced by REV
infection. The decreased phosphorylation level of ERK was associated with REV replication, suggesting that ERK signaling is involved in REV replication, and
allicin can alleviate the REV-induced immune dysfunction by inhibiting the activation of ERK. In addition, REV
infection induced oxidative damage in thymus and spleen, whereas
allicin treatment significantly decreased the oxidative stress induced by REV
infection, suggesting that the
antioxidant effect of
allicin should be at least partially responsible for the harmful effect of REV
infection. In conclusion, the findings suggest that
allicin alleviates the
inflammation and oxidative damage caused by REV
infection and exerts the potential anti-REV effect by blocking the ERK/MAPK pathway.