Phenoloxidase Is an Important Component of the Defense against Aeromonas hydrophila Infection in a Crustacean, Pacifastacus leniusculus

The melanization cascade, in which phenoloxidase is the terminal enzyme, appears to play a key role in recognition of and defense against microbial infections in invertebrates. Here, we show that phenoloxidase activity and melanization are important for the immune defense toward a highly pathogenic bacterium, Aeromonas hydrophila, in the freshwater crayfish, Pacifastacus leniusculus. RNA interference-mediated depletion of crayfish prophenoloxidase leads to increased bacterial growth, lower phagocytosis, lower phenoloxidase activity, lower nodule formation, and higher mortality when infected with this bacterium. In contrast, if RNA interference of pacifastin, an inhibitor of the crayfish prophenoloxidase activation cascade, is performed, it results in lower bacterial growth, increased phagocytosis, increased nodule formation, higher phenoloxidase activity, and delayed mortality. Our data therefore suggest that phenoloxidase is required in crayfish defense against an infection by A. hydrophila, a highly virulent and pathogenic bacterium to crayfish.

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A highly virulent pathogen, Aeromonas hydrophila, from the freshwater crayfish Pacifastacus leniusculus

Journal of Invertebrate Pathology ◽

10.1016/j.jip.2009.02.002 ◽

2009 ◽

Vol 101 (1) ◽

pp. 56-66 ◽

Cited By ~ 57

Author(s):

Pikul Jiravanichpaisal ◽

Stefan Roos ◽

Lennart Edsman ◽

Haipeng Liu ◽

Kenneth Söderhäll

Keyword(s):

Aeromonas Hydrophila ◽

Pacifastacus Leniusculus ◽

Freshwater Crayfish ◽

Highly Virulent

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Thioester-Containing Protein-4 Regulates the Drosophila Immune Signaling and Function against the Pathogen Photorhabdus

Journal of Innate Immunity ◽

10.1159/000450610 ◽

2016 ◽

Vol 9 (1) ◽

pp. 83-93 ◽

Cited By ~ 23

Author(s):

Upasana Shokal ◽

Ioannis Eleftherianos

Keyword(s):

Immune Response ◽

Photorhabdus Luminescens ◽

Human Pathogen ◽

Loss Of Function ◽

Phenoloxidase Activity ◽

Microbial Infections ◽

Immune Pathways ◽

And Function ◽

Important Progress

Despite important progress in identifying the molecules that participate in the immune response of Drosophila melanogaster to microbial infections, the involvement of thioester-containing proteins (TEPs) in the antibacterial immunity of the fly is not fully clarified. Previous studies mostly focused on identifying the function of TEP2, TEP3 and TEP6 molecules in the D. melanogaster immune system. Here, we investigated the role of TEP4 in the regulation and function of D. melanogaster host defense against 2 virulent pathogens from the genus Photorhabdus, i.e. the insect pathogenic bacterium Photorhabdus luminescens and the emerging human pathogen P. asymbiotica. We demonstrate that Tep4 is strongly upregulated in adult flies following the injection of Photorhabdus bacteria. We also show that Tep4 loss-of-function mutants are resistant to P. luminescens but not to P. asymbiotica infection. In addition, we find that inactivation of Tep4 results in the upregulation of the Toll and Imd immune pathways, and the downregulation of the Jak/Stat and Jnk pathways upon Photorhabdus infection. We document that loss of Tep4 promotes melanization and phenoloxidase activity in the mutant flies infected with Photorhabdus. Together, these findings generate novel insights into the immune role of TEP4 as a regulator and effector of the D. melanogaster antibacterial immune response.

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Updating the NLRC4 Inflammasome: from Bacterial Infections to Autoimmunity and Cancer

Frontiers in Immunology ◽

10.3389/fimmu.2021.702527 ◽

2021 ◽

Vol 12 ◽

Author(s):

Jiexia Wen ◽

Bin Xuan ◽

Yang Liu ◽

Liwei Wang ◽

Li He ◽

...

Keyword(s):

Bacterial Infections ◽

Molecular Mechanisms ◽

Protein Complexes ◽

Immune Defense ◽

Innate Immune ◽

Sensor Protein ◽

Different Types ◽

Microbial Infections ◽

Activation Mechanisms ◽

Specific Protease

Inflammasomes comprise a family of cytosolic multi-protein complexes that modulate the activation of cysteine-aspartate-specific protease 1 (caspase-1) and promote the maturation and secretion of interleukin (IL)-1β and IL-18, leading to an inflammatory response. Different types of inflammasomes are defined by their sensor protein which recognizes pathogenic ligands and then directs inflammasome assembly. Although the specific molecular mechanisms underlying the activation of most inflammasomes are still unclear, NLRC4 inflammasomes have emerged as multifaceted agents of the innate immune response, playing important roles in immune defense against a variety of pathogens. Other studies have also expanded the scope of NLRC4 inflammasomes to include a range of inherited human autoimmune diseases as well as proposed roles in cancer. In this review article, we provide an updated overview of NLRC4 inflammasomes, describing their composition, activation mechanisms and roles in both microbial infections and other disease conditions.

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Detection of Microbial Infections Through Innate Immune Sensing of Nucleic Acids

Annual Review of Microbiology ◽

10.1146/annurev-micro-102215-095605 ◽

2018 ◽

Vol 72 (1) ◽

pp. 447-478 ◽

Cited By ~ 100

Author(s):

Xiaojun Tan ◽

Lijun Sun ◽

Jueqi Chen ◽

Zhijian J. Chen

Keyword(s):

Nucleic Acid ◽

Nucleic Acids ◽

Immune Defense ◽

Innate Immune ◽

Type I Interferons ◽

Microbial Pathogens ◽

Type I ◽

Immune Recognition ◽

Microbial Infection ◽

Microbial Infections

Microbial infections are recognized by the innate immune system through germline-encoded pattern recognition receptors (PRRs). As most microbial pathogens contain DNA and/or RNA during their life cycle, nucleic acid sensing has evolved as an essential strategy for host innate immune defense. Pathogen-derived nucleic acids with distinct features are recognized by specific host PRRs localized in endolysosomes and the cytosol. Activation of these PRRs triggers signaling cascades that culminate in the production of type I interferons and proinflammatory cytokines, leading to induction of an antimicrobial state, activation of adaptive immunity, and eventual clearance of the infection. Here, we review recent progress in innate immune recognition of nucleic acids upon microbial infection, including pathways involving endosomal Toll-like receptors, cytosolic RNA sensors, and cytosolic DNA sensors. We also discuss the mechanisms by which infectious microbes counteract host nucleic acid sensing to evade immune surveillance.

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PHYSIOLOGICAL RESPONSES OF THE CRAYFISH PACIFASTACUS LENIUSCULUS TO ENVIRONMENTAL HYPEROXIA: I. EXTRACELLULAR ACID-BASE AND ELECTROLYTE STATUS AND TRANSBRANCHIAL EXCHANGE

Journal of Experimental Biology ◽

10.1242/jeb.143.1.33 ◽

1989 ◽

Vol 143 (1) ◽

pp. 33-51 ◽

Cited By ~ 1

Author(s):

MICHÉLE G. WHEATLY

Keyword(s):

Time Course ◽

Extracellular Fluid ◽

Respiratory Acidosis ◽

Pacifastacus Leniusculus ◽

Initial Increase ◽

Flux Analysis ◽

Freshwater Crayfish ◽

Acid Base ◽

Sequence Of Events ◽

Fluid Compartment

Extracellular acid--base and ionic status, and transbranchial exchange of acidic equivalents and electrolytes, were monitored in freshwater crayfish (Pacifastacus leniusculus) during control normoxia (PO2 = 148 mmHg; 1 mmHg = 133.3 Pa), 72 h of hyperoxia (PO2 = 500 mmHg) and 24 h of recovery. An initial (3 h) respiratory acidosis of 0.2 pH units was completely compensated within 48 h by a 50% increase in metabolic [HCO3−+CO32-] accompanied by a significant reduction in circulating [Cl−]. In addition, the original increase in Pco2 was partially accommodated. The time course of transbranchial acidic equivalent exchange paralleled the change in extracellular metabolic base load with a significant branchial output of H+ during the first 48 h of hyperoxia. This was associated with net branchial effluxes of Cl− and Mg2+. Unidirectional flux analysis revealed parallel reductions in Na+ influx and efflux during initial hyperoxic exposure, reflecting an alteration in exchange diffusion. The net Cl− efflux was due to an initial increase in efflux followed by a reduction in influx. The reverse sequence of events occurred more rapidly when normoxia was reinstated: metabolic base was removed from the haemolymph and control haemolymph acid--base and ion levels were re-established within 24 h. Transbranchial fluxes of acidic equivalents similarly recovered within 24 h although net Na+ output and Cl− uptake persisted. The study attempted to identify relationships between branchial net H+ exchange and components of Na+ and Cl− exchange and quantitatively to correlate changes in the acidic equivalent and electrolyte concentrations in the extracellular fluid compartment with those in the external water.

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Determinants of Immune Defense Against Microbial Infections: Santa Fe, New Mexico, February 24–29, 2000*

Viral Immunology ◽

10.1089/vim.2000.13.249 ◽

2000 ◽

Vol 13 (2) ◽

pp. 249-251

Author(s):

CAROL SHOSHKES REISS

Keyword(s):

New Mexico ◽

Immune Defense ◽

Santa Fe ◽

Microbial Infections

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Lipocalin 2: A New Antimicrobial in Mast Cells

International Journal of Molecular Sciences ◽

10.3390/ijms20102380 ◽

2019 ◽

Vol 20 (10) ◽

pp. 2380 ◽

Cited By ~ 2

Author(s):

Yu-Ling Chang ◽

Zhenping Wang ◽

Satomi Igawa ◽

Jae Eun Choi ◽

Tyler Werbel ◽

...

Keyword(s):

Mast Cells ◽

Antimicrobial Peptides ◽

Antimicrobial Peptide ◽

Bacterial Growth ◽

Immune Defense ◽

Lipocalin 2 ◽

Vitro Assay ◽

E Coli ◽

Sphingosine 1 Phosphate

Mast cells (MCs) play a significant role in the innate immune defense against bacterial infection through the release of cytokines and antimicrobial peptides. However, their antimicrobial function is still only partially described. We therefore hypothesized that MCs express additional antimicrobial peptides. In this study, we used FANTOM 5 transcriptome data to identify for the first time that MCs express lipocalin 2 (LCN2), a known inhibitor of bacterial growth. Using MCs derived from mice which were deficient in LCN2, we showed that this antimicrobial peptide is an important component of the MCs’ antimicrobial activity against Escherichia coli (E. coli). Since sphingosine-1-phosphate receptors (S1PRs) on MCs are known to regulate their function during infections, we hypothesized that S1P could activate LCN2 production in MCs. Using an in vitro assay, we demonstrated that S1P enhances MCs antimicrobial peptide production and increases the capacity of MCs to directly kill S. aureus and E. coli via an LCN2 release. In conclusion, we showed that LCN2 is expressed by MCs and plays a role in their capacity to inhibit bacterial growth.

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