Fish & shellfish immunology最新文献

Immune-reproductive interactions play important regulatory roles in vertebrate gonadal development. However, the contribution of immune factors to early gonadal development in teleost fish remains poorly understood. To address this, we conducted transcriptome profiling of male and female gonads in grass carp, a representative teleost species, across six developmental time points, focusing on the sex-biased development and immune-related genes. Our results pinpointed the initiation of molecular sex determination in grass carp at around 30 days post-fertilization (dpf), followed by ovarian and testicular morphological differentiation at approximately 60 and 120 dpf, respectively. Time-series analysis of differentially expressed genes (DEGs) revealed dynamic transcriptional changes associated with early gonadal differentiation, identifying key female- (e.g., cyp19a1a, foxl2a/b) and male-biased (e.g., dmrt1, amh) development-related genes. Interestingly, extensive sexual dimorphism was also observed in the expression of immune-related genes during early gonadal development. Specifically, females exhibited activation of early macrophage-related signaling (Stage 1) and late microenvironmental regulation (Stage 4), whereas males showed a delayed macrophage-related signaling (Stage 2) followed by a strong induction of type I interferon (IFN) signaling (Stage 3). Protein and protein interaction (PPI) network analysis further highlighted a divergence in regulatory architecture, demonstrating that ovarian hub genes were exclusively sex development-related (e.g., ccna1, fancd2) while testicular networks integrated both sex development and immune-related regulators (e.g., amh, isg15). Collectively, our findings characterize the dynamic and sex-specific coordination of developmental and immune programs, providing new insights into gonadal development in teleost.

Puffy Snout Syndrome (PSS) is an emerging, high-mortality condition of captive scombrids characterized by collagenous craniofacial overgrowth and tissue remodeling. Despite its prevalence in aquaculture, the molecular mechanisms underlying PSS remain unknown. Here, we performed mRNA and small RNA sequencing on facial tissues from wild-caught healthy, asymptomatic captive, and symptomatic captive Pacific mackerel (Scomber japonicus) to characterize transcriptional and post-transcriptional changes associated with the syndrome. Principal component analysis revealed strong separation between captive and wild groups, with symptomatic fish exhibiting the most pronounced transcriptional divergence. Across comparisons, 2,293 genes were differentially expressed, with symptomatic fish showing enrichment of cancer-associated pathways (e.g., Wnt signaling, extracellular matrix-receptor interactions) and immune processes including leukocyte activation and MAPK signaling. Asymptomatic fish also exhibited cancer-related and proliferative gene signatures, suggesting early molecular changes precede visible pathology. Key Wnt ligands (wnt9b, wnt3a, wnt10a) were overexpressed in captive groups, while immune effectors (ccl20a.4, perforin-1) were downregulated in symptomatic fish, indicating concurrent proliferative activation and immune suppression. MicroRNA profiling identified differential expression of tumor-suppressive gmo-let-7h-2, immune-regulatory ola-miR-223, and stress-responsive tni-miR-212, with predicted targets enriched for extracellular matrix organization, cytokine signaling, and neuronal processes. This study provides the first transcriptomic and miRNA evidence linking neoplastic signaling, immune dysregulation, and extracellular matrix remodeling to PSS. The detection of cancer-like molecular signatures in asymptomatic fish highlights potential for early diagnosis and monitoring. These findings establish a molecular framework for investigating PSS etiology, inform biomarker development, and underscore the need to evaluate environmental and infectious triggers in scombrid aquaculture.

Ammonia nitrogen (NH₃-N) pollution remains one of the most pervasive stressors threatening the health and productivity of modern aquaculture systems. Yet, its multi-level impacts on crustacean physiology are still incompletely understood. This study elucidates the morphological, biochemical, transcriptomic, and metabolomic responses of Macrobrachium rosenbergii gills to sublethal ammonia nitrogen exposure (0, 2, and 50 mg L^-1) over seven days. Histological observations revealed progressive gill deterioration characterized by epithelial lifting, lamellar fusion, and hemocytic infiltration. Antioxidant enzyme activities (SOD and CAT) increased adaptively under mild stress but were markedly suppressed under severe exposure, indicating oxidative dysfunction. Transcriptomic profiling uncovered extensive molecular remodeling, with 2207 and 1579 genes upregulated, and 2552 and 2191 downregulated in the 2 and 50 mg L^-1 groups, respectively (FDR <0.05). Differentially expressed genes were enriched in oxidative stress, nitrogen metabolism, apoptosis, and immune signaling pathways. Metabolomic analyses further revealed elevated citrulline and citric acid levels, reflecting disruptions in the urea cycle and energy metabolism. Integrative multi-omics analysis identified citrulline, citrate, GLUD1, NOS1, BCL2L1, MDA, and GSH as reliable biomarkers for early detection of ammonia stress. Collectively, these findings present a comprehensive mechanistic framework for understanding ammonia-induced toxicity in crustaceans and identify molecular indicators for improving health monitoring in sustainable aquaculture management.

Coagulation factors are crucial in physiological processes, including the progression of viral infections. However, the relationship between the coagulation cascade and viral hemorrhagic diseases in teleost fish remains poorly understood. In this study, grass carp coagulation factor 2 (F2) and its receptor protease-activated receptor 1(PAR1) were cloned and functionally characterized for their roles in response to grass carp reovirus (GCRV) infection. At the individual level, F2 expression was promptly upregulated during GCRV-Ⅱ infection, highlighting its involvement in the early immune response. At the cellular level, F2 overexpression enhanced viral replication, PAR1-mediated signaling, and apoptosis, whereas F2 knockdown significantly suppressed viral proliferation and reduced apoptosis. Furthermore, F2-mediated enhancement of apoptosis was shown to be dependent on PAR1 signaling. We further discovered that Serpine1, a major inhibitor of the fibrinolytic system, was strongly induced at the early stage of GCRV infection. Inhibition of Serpine1 led to reduced F2 and PAR1 expression, increased tPA and PLG levels, and suppressed viral replication. Together, these findings reveal a previously unrecognized Serpine1-F2-PAR1 signaling axis that links fibrinolysis-related gene regulation with virus-associated apoptosis and disease manifestations during GCRV infection. This study provides new insight into the interplay between coagulation-related pathways and viral pathogenesis in fish.