scholarly journals NOD2 and reproduction-associated NOD-like receptors have been lost during the evolution of pangolins

2021 ◽  
Author(s):  
Margarita Salova ◽  
Wolfgang Sipos ◽  
Erwin Tschachler ◽  
Leopold Eckhart
Keyword(s):  
Cell Biology ◽  
Mammalian Species ◽  
Muramyl Dipeptide ◽  
Skin Barrier ◽  
Innate Immune ◽  
Evolutionary Divergence ◽  
Immune Genes ◽  
Pyrin Domain ◽  
Innate Immune Genes ◽  
Molecular Patterns

AbstractNOD-like receptors (NLRs) are sensors of pathogen-associated molecular patterns with critical roles in the control of immune responses and programmed cell death. Recent studies have revealed inter-species differences in mammalian innate immune genes and a particular degeneration of nucleic acid sensing pathways in pangolins, which are currently investigated as potential hosts for zoonotic pathogens. Here, we used comparative genomics to determine which NLR genes are conserved or lost in pangolins and related mammals. We show that NOD2, which is implicated in sensing bacterial muramyl dipeptide and viral RNA, is a pseudogene in pangolins, but not in any other mammalian species investigated. NLRC4 and NAIP are absent in pangolins and canine carnivorans, suggesting convergent loss of cytoplasmic sensing of bacterial flagellin in these taxa. Among NLR family pyrin domain containing proteins (NLRPs), skin barrier-related NLRP10 has been lost in pangolins after the evolutionary divergence from Carnivora. Strikingly, pangolins lack all NLRPs associated with reproduction (germ cells and embryonic development) in other mammals, i.e., NLRP2, 4, 5, 7, 8, 9, 11, 13, and 14. Taken together, our study shows a massive degeneration of NLR genes in pangolins and suggests that these endangered mammals may have unique adaptations of innate immunity and reproductive cell biology.

1080 Milk yield genotype impacts expression of hepatic innate immune genes during the transition period in Holsteins

2016 ◽  
Vol 94 (suppl_5) ◽  
pp. 518-518
Author(s):  
G. T. Cousillas ◽  
W. J. Weber ◽  
B. Walcheck ◽  
D. E. Kerr ◽  
T. H. Elsasser ◽  
...  
Keyword(s):  
Milk Yield ◽  
Transition Period ◽  
Innate Immune ◽  
Immune Genes ◽  
Innate Immune Genes

Flagellin induces innate immune genes in bronchial epithelial cells in vivo: Role of TET2

2021 ◽  
Author(s):  
Wanhai Qin ◽  
Xanthe Brands ◽  
Cornelis Veer ◽  
Alex F. Vos ◽  
Brendon P. Scicluna ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Bronchial Epithelial Cells ◽  
Innate Immune ◽  
Bronchial Epithelial ◽  
Immune Genes ◽  
Innate Immune Genes

microRNA-252 and FoxO repress inflammaging by a dual inhibitory mechanism on Dawdle mediated TGF-β pathway in Drosophila

Genetics ◽  
2021 ◽  
Author(s):  
Xiaofen Wu ◽  
Kongyan Niu ◽  
Xiaofan Wang ◽  
Jing Zhao ◽  
Han Wang ◽  
...  
Keyword(s):  
Cell Types ◽  
Innate Immune ◽  
Low Grade ◽  
Sequencing Analysis ◽  
Immune Genes ◽  
Healthy Longevity ◽  
Muscle Tissues ◽  
Distinct Cell ◽  
A Cell ◽  
Innate Immune Genes

Abstract Inflammaging refers to low-grade, chronically activated innate immunity that has deleterious effects on healthy lifespan. However, little is known about the intrinsic signaling pathway that elicits innate immune genes during aging. Here using Drosophila melanogaster, we profile the microRNA targetomes in young and aged animals, and reveal Dawdle (Daw), an activin-like ligand of the TGF-β pathway, as a physiological target of microRNA-252 (miR-252). We show that miR-252 cooperates with Forkhead box O (FoxO), a conserved transcriptional factor implicated in aging, to repress Daw. Unopposed Daw triggers hyper activation of innate immune genes coupled with a decline in organismal survival. Using adult muscle tissues, single-cell sequencing analysis describes that Daw and its downstream innate immune genes are expressed in distinct cell types, suggesting a cell non-autonomous mode of regulation. We further determine the genetic cascade by which Daw signaling leads to increased Kenny/IKKγ protein, which in turn activates Relish/NF-κB protein and consequentially innate immune genes. Finally, transgenic increase of miR-252 and FoxO pathway factors in wild-type Drosophila extends lifespan and mitigates the induction of innate immune genes in aging. Together, we propose that miR-252 and FoxO promote healthy longevity by cooperative inhibition on Daw mediated inflammaging.

scholarly journals Modulatory upregulation of an insulin peptide gene by different pathogens in C. elegans

2017 ◽  
Author(s):  
Song-Hua Lee ◽  
Shizue Omi ◽  
Nishant Thakur ◽  
Clara Taffoni ◽  
Jérôme Belougne ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Signaling ◽  
Kinase Inhibitor ◽  
Innate Immune ◽  
Immune Genes ◽  
C Elegans ◽  
Intestinal Infections ◽  
Innate Immune Genes ◽  
Peptide Gene ◽  
Complex Manner

ABSTRACTWhen an animal is infected, its innate immune response needs to be tightly regulated across tissues and coordinated with other aspects of organismal physiology. Previous studies with Caenorhabditis elegans have demonstrated that insulin-like peptide genes are differentially expressed in response to different pathogens. They represent prime candidates for conveying signals between tissues upon infection. Here, we focused on one such gene, ins-11 and its potential role in mediating cross-tissue regulation of innate immune genes. While diverse bacterial intestinal infections can trigger the up-regulation of ins-11 in the intestine, we show that epidermal infection with the fungus Drechmeria coniospora triggers an upregulation of ins-11 in the epidermis. Using the Shigella virulence factor OpsF, a MAP kinase inhibitor, we found that in both cases, ins-11 expression is controlled cell autonomously by p38 MAPK, but via distinct transcription factors, STA-2/STAT in the epidermis and HLH-30/TFEB in the intestine. We established that ins-11, and the insulin signaling pathway more generally, are not involved in the regulation of antimicrobial peptide gene expression in the epidermis. The up-regulation of ins-11 in the epidermis does, however, affect intestinal gene expression in a complex manner, and has a deleterious effect on longevity. These results support a model in which insulin signaling, via ins-11, contributes to the coordination of the organismal response to infection, influencing the allocation of resources in an infected animal.

CF Monocyte Derived Macrophages Have an Attenuated Response to Extracellular Vesicles Secreted by Airway Epithelial Cells

2021 ◽  
Author(s):  
Katja Koeppen ◽  
Amanda B Nymon ◽  
Roxanna Barnaby ◽  
Zhongyou Li ◽  
Thomas H Hampton ◽  
...  
Keyword(s):  
Immune Response ◽  
Epithelial Cells ◽  
Bacterial Infection ◽  
Extracellular Vesicles ◽  
Cell Types ◽  
Airway Epithelial Cells ◽  
Innate Immune ◽  
Airway Epithelial ◽  
Immune Genes ◽  
Innate Immune Genes

Mutations in CFTR alter macrophage responses, for example, by reducing their ability to phagocytose and kill bacteria. Altered macrophage responses may facilitate bacterial infection and inflammation in the lungs, contributing to morbidity and mortality in cystic fibrosis (CF). Extracellular vesicles (EVs) are secreted by multiple cell types in the lungs and participate in the host immune response to bacterial infection, but the effect of EVs secreted by CF airway epithelial cells (AEC) on CF macrophages is unknown. This report examines the effect of EVs secreted by primary AEC on monocyte derived macrophages (MDM) and contrasts responses of CF and WT MDM. We found that EVs generally increase pro-inflammatory cytokine secretion and expression of innate immune genes in MDM, especially when EVs are derived from AEC exposed to Pseudomonas aeruginosa, and that this effect is attenuated in CF MDM. Specifically, EVs secreted by P. aeruginosa exposed AEC induced immune response genes and increased secretion of pro-inflammatory cytokines, chemoattractants and chemokines involved in tissue repair by WT MDM, but these effects were less robust in CF MDM. We attribute attenuated responses by CF MDM to differences between CF and WT macrophages because EVs secreted by CF AEC or WT AEC elicited similar responses in CF MDM. Our findings demonstrate the importance of AEC EVs in macrophage responses and show that the Phe508del mutation in CFTR attenuates the innate immune response of MDM to EVs.

scholarly journals Genomic architecture of haddock (Melanogrammus aeglefinus) shows expansions of innate immune genes and short tandem repeats

BMC Genomics ◽  
2018 ◽  
Vol 19 (1) ◽  
Author(s):  
Ole K. Tørresen ◽  
Marine S. O. Brieuc ◽  
Monica H. Solbakken ◽  
Elin Sørhus ◽  
Alexander J. Nederbragt ◽  
...  
Keyword(s):  
Short Tandem Repeats ◽  
Tandem Repeats ◽  
Innate Immune ◽  
Melanogrammus Aeglefinus ◽  
Immune Genes ◽  
Genomic Architecture ◽  
Innate Immune Genes ◽  
Haddock Melanogrammus Aeglefinus ◽  
Short Tandem

scholarly journals Molecular evolution in immune genes across the avian tree of life

2019 ◽  
Vol 5 ◽  
Author(s):  
Diana C. Outlaw ◽  
V. Woody Walstrom ◽  
Haley N. Bodden ◽  
Chuan-yu Hsu ◽  
Mark Arick ◽  
...  
Keyword(s):  
Purifying Selection ◽  
Tree Of Life ◽  
Innate Immune ◽  
Phylogenetic Study ◽  
Significant Differential Expression ◽  
Immune Genes ◽  
Treatment Groups ◽  
Show Evidence ◽  
Differential Gene ◽  
Innate Immune Genes

Abstract All organisms encounter pathogens, and birds are especially susceptible to infection by malaria parasites and other haemosporidians. It is important to understand how immune genes, primarily innate immune genes which are the first line of host defense, have evolved across birds, a highly diverse group of tetrapods. Here, we find that innate immune genes are highly conserved across the avian tree of life and that although most show evidence of positive or diversifying selection within specific lineages or clades, the number of sites is often proportionally low in this broader context of putative constraint. Rather, evidence shows a much higher level of negative or purifying selection in these innate immune genes – rather than adaptive immune genes – which is consistent with birds' long coevolutionary history with pathogens and the need to maintain a rapid response to infection. We further explored avian responses to haemosporidians by comparing differential gene expression in wild birds (1) uninfected with haemosporidians, (2) infected with Plasmodium and (3) infected with Haemoproteus (Parahaemoproteus). We found patterns of significant differential expression with some genes unique to infection with each genus and a few shared between ‘treatment’ groups, but none that overlapped with the genes included in the phylogenetic study.

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