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Developmental and Comparative Immunology
Pergamon Press
Developmental and Comparative Immunology

Pergamon Press

0145-305X

Developmental and Comparative Immunology/Journal Developmental and Comparative ImmunologySCIISTP
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    The costs and benefits of basal infection resistance vs immune priming responses in an insect

    Prakash, ArunAgashe, DeepaKhan, Imroze
    10页
    查看更多>>摘要:In insects, basal pathogen resistance and immune priming can evolve as mutually exclusive strategies, with distinct infection outcomes. However, the evolutionary drivers of such diverse immune functions remain poorly understood. Here, we addressed this key issue by systematically analyzing the differential fitness costs and benefits of priming vs resistance evolution in Tribolium beetle populations infected with Bacillus thuringiensis. Surprisingly, resistant beetles had increased post-infection reproduction and a longer lifespan under both starving as well as fed conditions, with no other measurable costs. In contrast, priming reduced offspring early survival, development rate and reproduction. Priming did improve post-infection survival of offspring, but this added trans-generational benefit of immune priming might not compensate for its pervasive costs. Resistance was thus consistently more beneficial. Overall, our work demonstrates the evolutionary change in trans-generational priming response, and provides a detailed comparison of the complex fitness consequences of evolved priming vs resistance.

    Litopenaeus vannamei peroxiredoxin 2-like is involved in WSSV infection by interaction with wsv089 and VP26

    Liu, Qing-HuiRen, Xing-ChaoLiu, Xiao-Ping
    9页
    查看更多>>摘要:White spot syndrome virus (WSSV) is one of the most dangerous pathogen in shrimp aquaculture, which can cause extremely high mortality of shrimp. A full understanding of virus-host interactions is important to prevent viral infection. In the present study, wsv089-interacting molecule Litopenaeus vannamei peroxiredoxins2-like (LvPrx2-L) was selected by the yeast two-hybrid (Y2H) method. The interaction between wsv089 and LvPrx2L was confirmed by far-western blotting assay. Interestingly, a further study indicated that LvPrx2-L interacted with VP26, and the molecular docking analysis supported the interaction between LvPrx2-L and VP26. Tissues distribution assay showed that LvPrx2-L was detected in all sampled tissues. The highest expression of LvPrx2-L was appeared in hemocytes. Following WSSV challenge, LvPrx2-L mRNA transcripts were significantly increased in the hemocytes and gill. In addition, the relative expression of IE1 and VP28 were remarkably upregulated in the hepatopancreas and intestines of LvPrx2-L-knockdown shrimp. Moreover, the cumulative survival rate was significantly lower in the LvPrx2-L- silenced group compared with the control and blank groups. Furthermore, LvPrx2-L could regulate the expression of proPO, crustin, ALF3, and CAT at the mRNA level. These findings would further deepen our understanding of WSSV-host interaction and shrimp antiviral response. All these data might useful for assessing the function of LvPrx2-L in the immune response of crustacean.

    Bombyx mori cypovirus (BmCPV) induces PINK1-Parkin mediated mitophagy via interaction of VP4 with host Tom40

    Xue, RenyuCao, GuangliZhu, MinPan, Jun...
    10页
    查看更多>>摘要:The mechanism by which infection by Bombyx mori cytoplasmic nucleopolyhedrosis virus (BmCPV) causes autophagy has not been studied in detail. Herein we have observed by electron microscopy that infection with BmCPV causes autophagosome and mitochondrial structure damage in Bombyx mori midgut. In BmN cells infected with BmCPV and expressing eGFP-LC3, fluorescence spots and LC3-II levels increased, suggesting that BmCPV infection causes autophagy. Autophagy inducer rapamycin (Rap) and autophagy inhibitor 3-methyladenine (3-MA) were used to monitor the effects of mitophagy on BmCPV proliferation. It was found BmCPV proliferation to be promoted by mitophagy. Transient transfection experiments in cultured BmN cells showed that mitophagy can be triggered by expression of BmCPV structural protein VP4. Moreover, VP4 caused upregulation of p-Drp1, PINK1 and Parkin proteins in the mitophagy pathway and downregulation of mitochondrial membrane protein Tom20. Furthermore, interaction between VP4 with Tom40 was confirmed by Co-IP, western blot and colocalization experiment, and overexpression of Tom40 reduce the level of mitochondrial autophagy induced by VP4. These results suggested that VP4 induced PINK1-Parkin-mediated mitophagy interacting with Tom40. These findings deepen our understanding of the interaction between BmCPV and silkworm and also provide a molecular target for screening anti-BmCPV drugs.

    Characterization and functional analysis of a clip domain serine protease (MncSP) and its alternative transcript (MncSP-isoform) from Macrobrachium nipponense

    Qin, WeiLu, YangWang, HongyuLiu, Beixiang...
    11页
    查看更多>>摘要:Clip domain serine protease (cSPs) play an important role in the innate immune defense of crustaceans. In this study, a clip domain serine protease (MncSP) and its alternative transcript (MncSP-isoform) were identified from Macrobrachium nipponense. The full-length cDNA sequences of MncSP and MncSP-isoform were 2447 and 2351 bp with open reading frames comprising 1497 and 1401 bp nucleotides and encoding 498 and 466 amino acids, respectively. The genome of MncSP had 10 exons and 9 introns. MncSP contained all 10 exons, whereas MncSP-isoform lacked the second exon. MncSP and MncSP-isoform contained a signal peptide, a clip domain, and a Tryp_SPc domain. Phylogenetic tree analysis showed that MncSP and MncSP-isoform clustered with cSPs from Palaemonidae. MncSP and MncSP-isoform were widely distributed in hemocytes, heart, hepatopancreas, gills, stomach, and intestine. The expression profiles of MncSP and MncSP-isoform in the hemocytes of M. nipponense changed after simulation by Vibrio parahaemolyticus or Staphylococcus aureus. The RNAi of MncSP could inhibit the expression of antimicrobial peptides (AMPs), including crustins and anti-lipopolysaccharide factors. Phe-noloxidase activity was also down-regulated in MncSP-silenced prawns. This study indicated that MncSP participated in the synthesis of AMPs and the activation of prophenoloxidase.

    Why and how do protective symbionts impact immune priming with pathogens in invertebrates?

    Beltran-Bech, SophieBraquart-Varnier, ChristinePrigot-Maurice, Cybele
    21页
    查看更多>>摘要:Growing evidence demonstrates that invertebrates display adaptive-like immune abilities, commonly known as "immune priming". Immune priming is a process by which a host improves its immune defences following an initial pathogenic exposure, leading to better protection after a subsequent infection with the same - or different - pathogens. Nevertheless, beneficial symbionts can enhance similar immune priming processes in hosts, such as when they face repeated infections with pathogens. This "symbiotic immune priming" protects the host against pathogenic viruses, bacteria, fungi, or eukaryotic parasites. In this review, we explore the extent to which protective symbionts interfere and impact immune priming against pathogens from both a mechanical (proximal) and an evolutionary (ultimate) point of view. We highlight that the immune priming of invertebrates is the cornerstone of the tripartite interaction of hosts/symbionts/pathogens. The main shared mechanism of immune priming (induced by symbionts or pathogens) is the sustained immune response at the beginning of hostmicrobial interactions. However, the evolutionary outcome of immune priming leads to a specific discrimination, which provides enhanced tolerance or resistance depending on the type of microbe. Based on several studies testing immune priming against pathogens in the presence or absence of protective symbionts, we observed that both types of immune priming could overlap and affect each other inside the same hosts. As protective symbionts could be an evolutionary force that influences immune priming, they may help us to better understand the heterogeneity of pathogenic immune priming across invertebrate populations and species.

    Immunomodulatory role of short neuropeptide F in the mud crab Scylla paramamosain

    Ye, HaihuiXu, ZhanningWei, YujieHuang, Huiyang...
    11页
    查看更多>>摘要:Short neuropeptide F (sNPF) is bioactive peptide secreted by neurons of invertebrates. It is one of the important pleiotropic neural molecules that is associated with a variety of physiological processes in invertebrates. However, little is known about the role of sNPF in the immune response. This study aimed to determine the distribution, localization, functional characteristics and signaling mechanisms of the sNPF gene and sNPF receptor (sNPF-R) gene in the mud crab Scylla paramamosain. Results of this study showed that Sp-sNPF and Sp-sNPF-R were widely expressed in neural tissue and other tissues including hemocytes. Further, in situ hybridization analysis revealed that Sp-sNPF and Sp-sNPF-R have specific localization in cerebral ganglion and hemocytes. It was also found that immune stimuli significantly induced Sp-sNPF expression in cerebral ganglion. The hemocyte-derived Sp-sNPF and Sp-sNPF-R were also efficiently activated upon immune stimulation. In vitro sNPF peptide administration enhanced phagocytic ability of hemocytes. However, this activity could be blocked through knockdown of sNPF-R-dsRNA or using adenylate cyclase inhibitors SQ 22536. The results of this study also demonstrated that the contents of signaling molecule adenylyl cyclase (AC), cyclic adenosine mono phosphate (cAMP) and protein kinase A (PKA) in hemocytes can be up-regulated after incubation with sNPF peptide. In addition, the results of in vivo experiments showed that sNPF increased concentration of nitric oxide (NO) and enhanced phagocytic potential in S. paramamosain. The sNPF also significantly induced the expression of immune-related molecules at the gene level in S. paramamosain. In conclusion, the findings of this study indicate that sNPF mediates hemocyte phagocytosis via sNPF-R receptor-coupled AC-cAMP-PKA pathway and influences the innate immune processes in S. paramamosain.

    A novel C-type lectin LvCTL 4.2 has antibacterial activity but facilitates WSSV infection in shrimp (L. vannamei)

    Huang, Yu-HsunLin, Shih-ShunWang, Han-ChingLiu, Chun-Hung...
    12页
    查看更多>>摘要:Glycan-binding protein C-type lectin (CTL), one of the pattern recognition receptors (PRRs), binds to carbohydrates on the surface of pathogens and elicits antimicrobial responses in shrimp innate immunity. The objective was to identify and characterize a novel C-type lectin LvCTL 4.2 in Litopenaeus vannamei. The LvCTL 4.2 protein consisted of a signal peptide at the N terminal and a carbohydrate-recognition domain (CRD) with a mutated mannose-binding (Glu-Pro-Ala; EPA) motif at the C terminal, and thereby has a putative secreted mannosebinding C-type lectin architecture. LvCTL 4.2 was highly expressed in nervous tissue and stomach. Infection with white spot syndrome virus (WSSV) induced expression of LvCTL 4.2 in shrimp stomach at 12 h post infection. Conversely, there was no obvious upregulation in expression of LvCTL 4.2 in stomach or hepatopancreas of shrimp with AHPND (acute hepatopancreas necrosis disease). Pathogen binding assays confirmed recombinant LvCTL 4.2 protein (rLvCTL 4.2) had significant binding ability with the WSSV virion, Gramnegative, and Gram-positive bacteria. Moreover, rLvCTL 4.2 had strong growth inhibition of Vibrio parahaemolyticus. Silencing LvCTL 4.2 suppressed WSSV replication, whereas pretreatment of WSSV with rLvCTL 4.2 facilitated viral replication in vivo. In conclusion, LvCTL 4.2 acted as a PRR that inhibited AHPND-causing bacteria, but facilitated WSSV pathogenesis.

    Hemeprotein amplifies the innate immune receptors of Ctenopharyngodon idellus kidney cells through NF-xB- and MAPK-dependent reactive oxygen species generation

    Li, JunLu, ZhijieTang, MeizhenZhang, Menglan...
    10页
    查看更多>>摘要:Infectious bacterial and viral diseases that cause hemolysis are considered life-threatening to grass carp (Ctenopharyngodon idellus), which is a species used in aquaculture worldwide. After heme and hemeproteins (Hb) are released as a result of hemolysis, the effect of excess Hb and heme on tissues remains to be characterized. To decipher the mechanisms, after incubation with Hb, we showed that lipopolysaccharide (LPS), Hb, and heme increased the cytotoxicity and secretion of inflammatory cytokines such as interleukin (IL)-6, chemokine (C-C motif) ligand 1 (CCL1), tumor necrosis factor (TNF)-a, IL-6, and IL-1I3 in vitro, which was due to stimulation of the expression of innate immune receptors, such as nucleotide-binding oligomerization domain (NOD2), toll-like receptor 2 (TLR2), TLR 4, and TLR3. The formation of reactive oxygen species (ROS) and the activation of mitogen-activated protein kinases (MAPKs) and nuclear factor (NF)-xB were important for increasing the cytokine production to induce heme, Hb, and LPS. Moreover, we confirmed that after LPS, Hb, and heme challenge, superoxide dismutase (SOD) and glutathione (GSH) synthetase (GSS) also caused remarkable destruction. However, catalase (CAT) and heme oxygenase-1 (HO-1) were strongly activated. In summary, our research findings present a framework through which heme and Hb concentrations amplify the secretions of inflammatory cytokines, which are induced by pattern recognition receptor (PRR) activation and present possible paths for immune intervention during infection with viral diseases and hemolytic bacterial.