Expression Of Chemokine CCL20 Research Articles

Effects of hypergravity exposure after 30-days simulated weightlessness on chemokine CCL20 and its receptor CCR6 in lingual mucosa of rhesus macaque

To study the influence of hypergravity exposure after 30-days simulated weightlessness on the expression of chemokine CCL20 and its receptor CCR6 in lingual mucosa of rhesus macaque. Twenty-three male rhesus monkeys were divided according to the random number method into one control group (A, n = 3) and three experimental groups, including the weightlessness group (B, n = 3), the hypergravity group (C, n = 3) and hypergravity exposure after 30-days simulated weightlessness group (D, n = 14), which was further divided into four subgroups according to the values of overload as: +11 Gx/270s group (D1, n = 3), +13 Gx/230s group (D2, n = 4) and +15 Gx/200s group (D3, n = 4) and +13 Gx/230s with 9-days recovery group (D4, n = 3). Histopathological changes of lingual mucosa were observed by hematoxylin-eosin staining and the expressions of CCL20 and CCR6 were detected by immunohistochemistry (IHC) and quantitative real-time PCR (Q-PCR). Histological observation showed that no significant histopathological changes were found in the lingual mucosa in all experimental groups of the animals, however, there were more infiltrated lymphocyte and neutrophils in the experimental groups. The immunohistochemical scores of CCL20 in group C, group D2 and group D3 were 1.30 ± 0.11, 1.68 ± 0.62 and 2.26 ± 1.00, respectively, significantly higher than that in A group (0.47 ± 0.12, P < 0.05). The immunohistochemical scores of CCR6 expression in those three groups were 4.40 ± 1.48, 6.67 ± 2.04 and 7.02 ± 2.11, respectively, also remarkably higher than that in A group (1.33 ± 0.66, P < 0.05). As far as the mRNA expression was concerned, the expressions of CCL20 and CCR6 had similar change trend with their protein expressions. Hypergravity exposure after 30-days simulated weightlessness will not lead to significant pathological changes in lingual mucosa, but can induce the expression of chemokine CCL20 and its receptor CCR6.

Induction of CCL20 production by Kaposi sarcoma–associated herpesvirus: role of viral FLICE inhibitory protein K13-induced NF-κB activation

AbstractKaposi sarcoma–associated herpesvirus (KSHV), also known as human herpesvirus 8, is the etiologic agent of Kaposi sarcoma (KS), an angioproliferative lesion characterized by dramatic angiogenesis and inflammatory infiltration. In this study, we report that expression of chemokine CCL20, a potent chemoattractant of dendritic cells and lymphocytes, is strongly induced in cultured cells either by KSHV infection or on ectopic expression of viral FLICE inhibitory protein K13. This induction is caused by transcriptional activation of CCL20 gene, which is mediated by binding of the p65, p50, and c-Rel subunits of the transcription factor nuclear factor–κB (NF-κB) to an atypical NF-κB–binding site present in the CCL20 gene promoter. The CCL20 gene induction is defective in K13 mutants that lack NF-κB activity, and can be blocked by specific genetic and pharmacologic inhibitors of the NF-κB pathway. CCR6, the specific receptor for CCL20, is also induced in cultured cells either by KSHV infection or on K13 expression. Finally, expression of CCL20 and CCR6 is increased in clinical samples of KS. These results suggest that KSHV and K13-mediated induction of CCL20 and CCR6 may contribute to the recruitment of dendritic cells and lymphocytes into the KS lesions, and to tumor growth and metastases.