Transcriptome sequencing reveals phagocytosis as the main immune response in the pathogen-challenged sea urchin Strongylocentrotus intermedius.

The clarification of host immune responses to causative bacteria of spotting disease in the sea urchin Strongylocentrotus intermedius is vital to preventing and controlling this disease, especially to selective breeding for disease resistance. For this purpose, sea urchins were challenged with the causative bacterium Vibrio sp. to obtain spotting diseased and undiseased samples. We conducted next-generation sequencing to assess the key genes/pathways in control (CG), diseased (DG), and undiseased (UG) groups. A total of 454.1 million clean reads were obtained and assembled into 23,899 UniGenes with an N50 of 1359 bp, with 86.11% of them matching the genome sequence of the sea urchin S. purpuratus. A total of 8415 UniGenes were mapped to the non-redundant database. Salmon expression analysis revealed 725 significantly differentially expressed genes (DEGs) among CG, DG, and UG. These DEGs were enriched into 72 Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways, including a core set of immune correlated pathways notably in the phagosome, vitamin digestion and absorption, Wnt signaling, and Notch signaling pathways. DG was evidently upregulated in these immune pathways and could enhance phagocytosis directly or indirectly. Thus, phagocytosis was the main coelomic cellular immune response in S. intermedius challenged by spotting disease causative bacterium. The expression patterns of 10 DEGs were confirmed via RT-qPCR, and the expression levels were consistent with the results of RNA-seq. Furthermore, 9899 SSRs were identified, and 123,692, 151,827, and 114,368 candidate SNPs were identified from CG, DG, and UG, respectively. These results provide basic information for our understanding of sea urchin antibacterial immunity.

Comparison of Immune Indicators Related to Phagocytosis of Five Species of Sea Urchins under Artificial Infection with the Pathogenic Bacterium of Black Mouth Disease.

To screen for immune indicators closely related to disease resistance, two species of sea urchin susceptible to black mouth disease (Strongylocentrotus intermedius, S. intermedius ♀ × Heliocidaris crassispina ♂) and three species of sea urchin resistant to black mouth disease (H. crassispina, H. crassispina ♀ × S. intermedius ♂ and Mesocentrotus nudus) were artificially infected with the black mouth pathogen Vibrio echinoideorum. The phagocytosis-related immune indices of the five sea urchin species were compared at different time points post-infection. The results demonstrated that the parameters such as apoptotic rate of phagocytes, mean contribution value (MCV) of single effective phagocyte on Acid Phosphatase (ACP), Reactive Oxygen Species (ROS), and Total Antioxidant Capacity (T-AOC) of the five sea urchin species first increased and then decreased after infection. The key time points were 3 h to 6 h and 48 h post-infection when the black mouth disease-resistant and susceptible sea urchins demonstrated differences. At 3 h or 6 h post-infection, the up-regulation folds in MCV of ACP, ROS and T-AOC of black mouth disease-resistant sea urchins were considerably higher than that of the susceptible sea urchins. At 6 h post-infection, the apoptosis rate and the phagocytic index (PI) of the black mouth disease-resistant sea urchins were significantly higher than those of the susceptible sea urchins (p < 0.05). At 48 h post-infection, the necrosis rate of phagocytes, MCV of ACP and MCV of ROS of the black mouth disease-resistant sea urchins were significantly lower than those of the susceptible sea urchins (p < 0.05). The apoptosis and necrosis rate of phagocytes, PI, and MCV on ACP, ROS may be used as indicators of disease resistance in sea urchins. Disease resistance standards in immune indices can be summarized as phagocytosis increases greatly in the early infection stage and decreases timely to a normal level after killing the pathogen in a short period.

Comprehensive Analysis Identifies the PPAR-Targeted Genes Associated with Ovarian Cancer Prognosis and Tumor Microenvironment.

Background: There is a significant role for peroxisome proliferator-activated receptors (PPARs) in the development of cancer. Nevertheless, the role of PPARs-related genes in ovarian cancer (OC) remains unclear. Methods: The open-accessed data used for analysis were downloaded from The Cancer Genome Atlas database, which was analyzed using the R software. Results: In our study, we comprehensively investigated the PPAR target genes in OC, including their biological role. Meanwhile, a prognosis signature consisting of eight PPAR target genes was established, including apolipoprotein A-V, UDP glucuronosyltransferase 2 family, polypeptide B4, TSC22 domain family, member 1, growth hormone inducible transmembrane protein, renin, dedicator of cytokinesis 4, enoyl CoA hydratase 1, peroxisomal (ECH1), and angiopoietin-like 4, which showed a good prediction efficiency. A nomogram was constructed by combining the clinical feature and risk score. Immune infiltration and biological enrichment analysis were applied to investigate the difference between high- and low-risk patients. Immunotherapy analysis indicated that low-risk patients might respond better to immunotherapy. Drug sensitivity analysis indicated that high-risk patients might respond better to bleomycin, nilotinib, pazopanib, pyrimethamine, and vinorelbine, yet worse to cisplatin and gefitinib. Furthermore, the gene ECH1 was selected for further analysis. Conclusions: Our study identified a prognosis signature that could effectively indicates patients survival. Meanwhile, our study can provide the direction for future studies focused on the PPARs in OC.