Recently, gut microbiota for various pathogens has attracted attention. The present study investigated the role of gut microbiota unmethylated cytosine phosphate guanine DNA (CpG-DNA) on liver Kupffer cells (KCs) inflammatory cytokine interleukin-1β (IL-1β) in diabetic rats. We induced diabetic rats models and sequenced the gut microbiota composition of fecal samples. We also applied CpG-DNA and TLR9 inhibitor on KCs to investigate the regulation of inflammatory cytokine IL-1β and Toll-like receptor 9 (TLR9) signaling pathway. We found a significant difference of gut microbiota between the control and the diabetic rats with increased Clostridium. Meanwhile, diabetes could upregulate TLR9 in KCs and increase IL-1β concentration. Furthermore, high concentration of unmethylated CpG-DNA could significantly increase IL-1β secretion while it was suppressed by TLR9 inhibitor in KCs cultured in high glucose medium. Our study suggests that unmethylated CpG-DNA, which was highly expressed in diabetic rats, activated KCs through TLR9, and induced IL-1β secretion in vitro and in vivo which plays an important role in diabetic liver inflammation. It may contribute to the progress of the diabetes.
Figure 1
Figure 2
Figure 3
Figure 4
Loading...
Posted 12 Mar, 2021
Received 07 Mar, 2021
Invitations sent on 04 Mar, 2021
On 01 Mar, 2021
On 25 Feb, 2021
Posted 12 Mar, 2021
Received 07 Mar, 2021
Invitations sent on 04 Mar, 2021
On 01 Mar, 2021
On 25 Feb, 2021
Recently, gut microbiota for various pathogens has attracted attention. The present study investigated the role of gut microbiota unmethylated cytosine phosphate guanine DNA (CpG-DNA) on liver Kupffer cells (KCs) inflammatory cytokine interleukin-1β (IL-1β) in diabetic rats. We induced diabetic rats models and sequenced the gut microbiota composition of fecal samples. We also applied CpG-DNA and TLR9 inhibitor on KCs to investigate the regulation of inflammatory cytokine IL-1β and Toll-like receptor 9 (TLR9) signaling pathway. We found a significant difference of gut microbiota between the control and the diabetic rats with increased Clostridium. Meanwhile, diabetes could upregulate TLR9 in KCs and increase IL-1β concentration. Furthermore, high concentration of unmethylated CpG-DNA could significantly increase IL-1β secretion while it was suppressed by TLR9 inhibitor in KCs cultured in high glucose medium. Our study suggests that unmethylated CpG-DNA, which was highly expressed in diabetic rats, activated KCs through TLR9, and induced IL-1β secretion in vitro and in vivo which plays an important role in diabetic liver inflammation. It may contribute to the progress of the diabetes.
Figure 1
Figure 2
Figure 3
Figure 4
Loading...