scholarly journals Defective apoptotic cell clearance activates innate immune response to protect Caenorhabditis elegans against pathogenic bacteria

Virulence ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 75-83
Author(s):  
Jinlong Wan ◽  
Lei Yuan ◽  
Huiru Jing ◽  
Qian Zheng ◽  
Hui Xiao
Keyword(s):  
Immune Response ◽  
Caenorhabditis Elegans ◽  
Innate Immune Response ◽  
Pathogenic Bacteria ◽  
Apoptotic Cell ◽  
Innate Immune ◽  
Apoptotic Cell Clearance ◽  
Cell Clearance

scholarly journals PtdIns(4,5)P2 and PtdIns3P coordinate to regulate phagosomal sealing for apoptotic cell clearance

2015 ◽  
Vol 210 (3) ◽  
pp. 485-502 ◽  
Author(s):  
Shiya Cheng ◽  
Kun Wang ◽  
Wei Zou ◽  
Rui Miao ◽  
Yaling Huang ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Apoptotic Cell ◽  
Pi3 Kinase ◽  
Coincidence Detection ◽  
Dynamic Changes ◽  
Detection Mechanism ◽  
Close Coupling ◽  
Apoptotic Cell Clearance ◽  
Cell Clearance ◽  
Family Protein

Phagocytosis requires phosphoinositides (PIs) as both signaling molecules and localization cues. How PIs coordinate to control phagosomal sealing and the accompanying switch of organelle identity is unclear. In this study, we followed dynamic changes in PIs during apoptotic cell clearance in Caenorhabditis elegans. We found that phosphatidylinositol-4,5-bisphosphate (PtdIns(4,5)P2) and phosphatidylinositol-3-phosphate (PtdIns3P), which accumulate transiently on unsealed and fully sealed phagosomes, respectively, are both involved in phagosome closure. We identified PtdIns3P phosphatase MTM-1 as an effector of PtdIns(4,5)P2 to promote phagosomal sealing. MTM-1 coordinates with the class II PI3 kinase PIKI-1 to control PtdIns3P levels on unsealed phagosomes. The SNX9 family protein LST-4 is required for sealing, and its association with unsealed phagosomes is regulated by PtdIns(4,5)P2, PIKI-1, and MTM-1. Loss of LST-4 or its retention on phagosomes disrupts sealing and suppresses PtdIns3P accumulation, indicating close coupling of the two events. Our findings support a coincidence detection mechanism by which phagosomal sealing is regulated and coupled with conversion from PtdIns(4,5)P2 enrichment on unsealed phagosomes to PtdIns3P enrichment on fully sealed phagosomes.

Loss of DNase II function in the gonad is associated with a higher expression of antimicrobial genes in Caenorhabditis elegans

2015 ◽  
Vol 470 (1) ◽  
pp. 145-154 ◽  
Author(s):  
Hsiang Yu ◽  
Huey-Jen Lai ◽  
Tai-Wei Lin ◽  
Chang-Shi Chen ◽  
Szecheng J. Lo
Keyword(s):  
Immune Response ◽  
Innate Immunity ◽  
Caenorhabditis Elegans ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Dnase Ii ◽  
C Elegans ◽  
Elevated Expression

This study uncovered NUC-1 and CRN-7 function in germline apoptosis. Mutations of nuc-1 and crn-7 led to elevated expression of five innate-immunity-related genes and demonstrated that DNase II activity is associated with an innate immune response in C. elegans.

scholarly journals Clathrin and AP2 Are Required for Phagocytic Receptor-Mediated Apoptotic Cell Clearance in Caenorhabditis elegans

PLoS Genetics ◽  
2013 ◽  
Vol 9 (5) ◽  
pp. e1003517 ◽  
Author(s):  
Didi Chen ◽  
Youli Jian ◽  
Xuezhao Liu ◽  
Yuanya Zhang ◽  
Jingjing Liang ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Apoptotic Cell ◽  
Apoptotic Cell Clearance ◽  
Cell Clearance

Innate immune response of bovine mammary gland to pathogenic bacteria responsible for mastitis

2007 ◽  
Vol 54 (4) ◽  
pp. 399-409 ◽  
Author(s):  
Javier Oviedo-Boyso ◽  
Juan J. Valdez-Alarcón ◽  
Marcos Cajero-Juárez ◽  
Alejandra Ochoa-Zarzosa ◽  
Joel E. López-Meza ◽  
...  
Keyword(s):  
Immune Response ◽  
Mammary Gland ◽  
Innate Immune Response ◽  
Pathogenic Bacteria ◽  
Innate Immune ◽  
Bovine Mammary Gland

scholarly journals Analysis of the Caenorhabditis elegans innate immune response to Coxiella burnetii

2016 ◽  
Vol 23 (2) ◽  
pp. 111-127 ◽  
Author(s):  
James M Battisti ◽  
Lance A Watson ◽  
Myo T Naung ◽  
Adam M Drobish ◽  
Ekaterina Voronina ◽  
...  
Keyword(s):  
Immune Response ◽  
Caenorhabditis Elegans ◽  
Innate Immune Response ◽  
Coxiella Burnetii ◽  
Molecular Mechanisms ◽  
Q Fever ◽  
Innate Immune ◽  
Human Pathogens ◽  
C Elegans ◽  
Intestinal Distension

The nematode Caenorhabditis elegans is well established as a system for characterization and discovery of molecular mechanisms mediating microbe-specific inducible innate immune responses to human pathogens. Coxiella burnetii is an obligate intracellular bacterium that causes a flu-like syndrome in humans (Q fever), as well as abortions in domesticated livestock, worldwide. Initially, when wild type C. elegans (N2 strain) was exposed to mCherry-expressing C. burnetii (CCB) a number of overt pathological manifestations resulted, including intestinal distension, deformed anal region and a decreased lifespan. However, nematodes fed autoclave-killed CCB did not exhibit these symptoms. Although vertebrates detect C. burnetii via TLRs, pathologies in tol-1(–) mutant nematodes were indistinguishable from N2, and indicate nematodes do not employ this orthologue for detection of C. burnetii. sek-1(–) MAP kinase mutant nematodes succumbed to infection faster, suggesting that this signaling pathway plays a role in immune activation, as previously shown for orthologues in vertebrates during a C. burnetii infection. C. elegans daf-2(–) mutants are hyper-immune and exhibited significantly reduced pathological consequences during challenge. Collectively, these results demonstrate the utility of C. elegans for studying the innate immune response against C. burnetii and could lead to discovery of novel methods for prevention and treatment of disease in humans and livestock.

scholarly journals Pediococcus acidilactici P25 Protected Caenorhabditis elegans against Enterotoxigenic Escherichia coli K88 Infection and Transcriptomic Analysis of Its Potential Mechanisms

2020 ◽  
Vol 2020 ◽  
pp. 1-17 ◽  
Author(s):  
Keqin Tan ◽  
Dun Deng ◽  
Xianyong Ma ◽  
Yiyan Cui ◽  
Zhimei Tian
Keyword(s):  
Escherichia Coli ◽  
Immune Response ◽  
Caenorhabditis Elegans ◽  
Bile Salt ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Mitogen Activated Protein Kinase ◽  
Enterotoxigenic Escherichia Coli ◽  
Pediococcus Acidilactici ◽  
Enterotoxin Genes

Enterotoxigenic Escherichia coli (ETEC) K88 is a zoonotic pathogen. Previous studies have shown that lactic acid bacteria (LAB) have great potential in promoting health and resisting pathogenic infections; however, relatively little research has been done on the Pediococcus genus of LAB. This study is aimed at exploring the mechanisms imparted by Pediococcus acidilactici P25 against ETEC K88 in Caenorhabditis elegans. The probiotic performance of P25 was investigated in vitro. Colonization of K88 in the intestinal tract of C. elegans and abundance of enterotoxin genes were measured. In addition, the transcriptome of C. elegans infected by K88 was analyzed. The result showed that P25 possessed the ability to produce acid, as well as high tolerances to acidic and high bile salt concentrations. Coculture revealed that the growth of ETEC K88 was significantly inhibited by the presence of P25. The median survival of C. elegans fed P25 was 2 days longer than the group infected with K88 alone (P<0.01). At the same time, the number of colonizing K88 and the abundances of estB and elt were reduced by up to 71.70% and 2.17 times, respectively, by P25. Transcriptome data indicated that P25 affected expression of genes relative to innate immune response and upregulated the abundance of genes in multiple pathways of C. elegans, including peroxisome, longevity, and mitogen-activated protein kinase (MAPK) pathways. These results demonstrated that in the presence of P25, K88 colonization and their expression of enterotoxin genes were reduced. This was accomplished through the alteration of environmental parameters (pH and bile salt) as well as through the promotion of the innate immune response processes, increased longevity, and increased antipathogenic bacteria-related pathways. This work highlights the potential application of P. acidilactici P25 as a probiotic resistant to ETEC K88.

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