TsTPX2 Regulates Th2 Immune Response trichinosis. Our study showed that TsTPX2 would be at least one of the molecules to switch macrophages into the M2 phenotype during T. spiralis infection, which provides a new therapeutic approach to various inflammatory disorders like allergies or autoimmune diseases.
Background Both of American mink (Neovison vison) and wild rat (Rattus norvegicus) is considered reservoir hosts carrying many endoparasites. Trichinella is a successful parasitic nematode including nine species and three genotypes with a worldwide distribution. However, little is known about the prevalence of Trichinella infection in mink (Neovison vison) and rat (Rattus norvegicus) in China.Methods In total, 289 muscle samples of minks and 102 rat carcasses were collected between April 2017 and December 2019 in Weihai city of Shandong province, China. The food of minks including chicken skeleton and mashed marine products was also collected at 3 batches. All the samples were used to examine for the appearance of Trichinella by the pooled artificial HCl-pepsin digestion method. The isolates from minks and rats were identified as T. spiralis by multiplex PCR. Then, the phylogenetic tree was constructed based on the sequences of 5S rDNA inter-gene spacer regions.Results Muscle larvae were detected in 20 out of 289 minks (6.92%) and in 2 of 102 wild rats (1.96%), respectively. The intensity of Trichinella in mink samples was ranged from 0.025 to 0.815 lpg, while the larval burden in rats was 0.17 lpg. The isolates from minks and rats were identified as T. spiralis by multiplex PCR. Sequence analysis revealed a 100% identical alignment of the 5S rDNA inter-gene spacer regions from the two isolates. The phylogenetic tree confirmed the two isolates from minks and rats belonging to T. spiralis based on analysis of the 5S rDNA inter-gene spacer sequence.Conclusions The present study represents the first report of T. spiralis infection in American mink (Neovison vison) and wild rat (Rattus norvegicus) from Shandong province, China. The farmed minks would be vulnerable to Trichinella infection through exposure to the wild rats. The prevalence of T. spiralis in wild rats may raise a public health concern for the potential zoonotic risk for the domestic animals.
cGAS-STING signaling is a major pathway in inducing type Ⅰ IFN, which plays a crucial role in the defense against T. gondii infection. In contrast, T. gondii develops multiple strategies to counteract the host defense, causing serious diseases in a wide range of hosts. Here, we demonstrate that T. gondii rhoptry protein 16 (ROP16) dampens type I interferon signaling via the inhibition of the cGAS (cyclic GMP-AMP synthase) pathway through the polyubiquitination of STING. Mechanistically, ROP16 interacts with STING through the SignalP domain and inhibits the K63-linked ubiquitination of STING in an NLS (nuclear localization signal)-domain-dependent manner. Consequently, knocking out the ROP16 in PRU tachyzoites promotes the STING-mediated production of type I IFNs and limits the replication of T. gondii. Together, these findings describe a distinct pathway where T. gondii exploits the ubiquitination of STING to evade host anti-parasite immunity, revealing new insights into the interaction between the host and parasites.
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