Polymorphism of TLR2 in bank vole populations in North Eastern Poland is not associated with Borrelia afzelii infection prevalence

Abstract Polymorphism in innate immune genes in host populations can structure spatial variation in the prevalence of infectious diseases. In Europe, Borrelia afzelii is an important tick-borne pathogen of small mammals including the bank voles (Myodes glareolus). The Toll-like receptor 2 (TLR2) is an innate immune receptor that is important for detecting Borrelia burgdorferi sensu lato pathogens. The TLR2 gene is polymorphic in bank vole populations and is classified into four distinct clusters: C1, C2, C3, and C4. The C2 and C4 clusters versus the C1 and C3 clusters are associated with lower versus higher infection prevalence, respectively. We detected three TLR2 clusters in 487 bank voles from 30 populations in NE Poland: 84.2% of the obtained sequences belonged to the C1 variant, 7.2% to C2, and 8.6% to C3. However, no clear spatial structure of TLR2 clusters among the populations was detected. B. afzelii infection prevalence across all studied individuals was 12.1% and varied from 0 to 37.5% among populations. There were no significant differences in B. afzelii prevalence among voles carrying alleles of different TLR2 clusters, or between individuals belonging to two mtDNA lineages. Most infected individuals were adults, and males were infected more often than females. There was no significant relationship between the prevalence of TLR2 clusters in the vole populations and climatic and environmental factors within the study area. We therefore could not confirm an adaptive role of the TLR2 C2 alleles in reducing B. afzelii infection prevalence in bank voles.

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Borrelia afzelii does not suppress the development of anti-tick immunity in bank voles

10.1101/2020.03.31.018754 ◽

2020 ◽

Author(s):

Andrea Gomez-Chamorro ◽

Yating Li ◽

Adrian Herrera ◽

Olivier Rais ◽

Hans Dautel ◽

...

Keyword(s):

Bank Vole ◽

Myodes Glareolus ◽

Acquired Immunity ◽

Salivary Gland Extract ◽

Borrelia Afzelii ◽

Tick Vector ◽

Bank Voles ◽

Gland Extract ◽

Tick Transmission ◽

Vertebrate Hosts

AbstractVector-borne pathogens manipulate their vertebrate hosts to enhance their transmission to arthropod vectors. The ability of vertebrate hosts to develop acquired immunity against arthropod vectors represents an existential threat for both the vector and the pathogen. The purpose of the study was to test whether the tick-borne spirochete bacterium Borrelia afzelii could suppress the development of acquired immunity to its tick vector Ixodes ricinus in the bank vole Myodes glareolus, which is an important host for both the tick and the pathogen. We created a group of B. afzelii-infected bank voles and an uninfected control group by exposing lab-reared animals to infected or uninfected ticks. At 1, 2, and 3 months post-infection, all bank voles were infested with larval I. ricinus ticks. The bank voles developed a strong antibody response against tick salivary gland extract proteins. This anti-tick immunity had negative effects on tick fitness traits including engorged larval weight, unfed nymphal weight, larva-to-nymph molting time and larva-to-nymph molting success. Infection with B. afzelii did not suppress the development of acquired immunity against I. ricinus ticks. The development of anti-tick immunity was strongly correlated with a dramatic temporal decline in both the bacterial abundance in the host ear tissues and the host-tick transmission success of B. afzelii. Our study suggests that the development of anti-tick immunity in bank voles has important consequences for the density of infected ticks and the risk of Lyme borreliosis.ImportanceMany pathogens enhance their persistence and transmission by suppressing the immune system of their host. We used an experimental infection approach to test whether the Lyme disease pathogen, Borrelia afzelii, could suppress the development of acquired immunity against its tick vector (Ixodes ricinus) in the bank vole (Myodes glareolus), but found no evidence for this phenomenon. Uninfected and B. afzelii-infected bank voles both developed a strong IgG antibody response against tick salivary gland extract following repeated infestations with I. ricinus ticks. The development of anti-tick immunity was negatively correlated with the abundance of B. afzelii in ear tissue biopsies and with host-to-tick transmission to I. ricinus ticks. Our study suggests that anti-tick immunity in the bank vole reduces the prevalence of this important tick-borne pathogen.

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

Journal of Animal Science ◽

10.2527/jam2016-1080 ◽

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

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

Scandinavian Journal of Immunology ◽

10.1111/sji.13046 ◽

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

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

Genetics ◽

10.1093/genetics/iyab234 ◽

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.

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

10.1101/238568 ◽

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.

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

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00621.2020 ◽

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.

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Association Of Polymorphisms In Known And Novel Innate Immune Genes With Gram Negative Bacteremia

10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3869 ◽

2011 ◽

Cited By ~ 1

Author(s):

Ivana V. Yang ◽

Laura A. Warg ◽

Scott Alper ◽

David A. Schwartz

Keyword(s):

Innate Immune ◽

Gram Negative ◽

Immune Genes ◽

Gram Negative Bacteremia ◽

Innate Immune Genes

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Responses of some innate immune‐genes involved in the toll‐pathway in black tiger shrimp ( Penaeus monodon ) to Vibrio harveyi infection and on exposure to ligands in vitro

Journal of the World Aquaculture Society ◽

10.1111/jwas.12723 ◽

2020 ◽

Vol 51 (6) ◽

pp. 1419-1429 ◽

Cited By ~ 1

Author(s):

Anand Deepika ◽

Krishnan Sreedharan ◽

Kooloth Valappil Rajendran

Keyword(s):

Vibrio Harveyi ◽

Penaeus Monodon ◽

Innate Immune ◽

Toll Pathway ◽

Immune Genes ◽

Black Tiger Shrimp ◽

Tiger Shrimp ◽

Innate Immune Genes

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Bank vole immunoheterogeneity may limit Nephropatia Epidemica emergence in a French non-endemic region

Parasitology ◽

10.1017/s0031182017001548 ◽

2017 ◽

Vol 145 (3) ◽

pp. 393-407 ◽

Cited By ~ 6

Author(s):

A. DUBOIS ◽

G. CASTEL ◽

S. MURRI ◽

C. PULIDO ◽

J.-B. PONS ◽

...

Keyword(s):

Bank Vole ◽

Myodes Glareolus ◽

Disease Emergence ◽

Endemic Region ◽

Natural Reservoir ◽

Bank Voles ◽

Free Region ◽

Limited Dispersal ◽

Antiviral Gene ◽

French Region

SUMMARYEcoevolutionary processes affecting hosts, vectors and pathogens are important drivers of zoonotic disease emergence. In this study, we focused on nephropathia epidemica (NE), which is caused by Puumala hantavirus (PUUV) whose natural reservoir is the bank vole,Myodes glareolus. We questioned the possibility of NE emergence in a French region that is considered to be NE-free but that is adjacent to a NE-endemic region. We first confirmed the epidemiology of these two regions and we demonstrated the absence of spatial barriers that could have limited dispersal, and consequently, the spread of PUUV into the NE-free region. We next tested whether regional immunoheterogeneity could impact PUUV chances to circulate and persist in the NE-free region. We showed that bank voles from the NE-free region were sensitive to experimental PUUV infection. We observed high levels of immunoheterogeneity between individuals and also between regions. Antiviral gene expression (TnfandMx2) reached higher levels in bank voles from the NE-free region. During experimental infections, anti-PUUV antibody production was higher in bank voles from the NE-endemic region. These results indicated a lower susceptibility to PUUV for bank voles from this NE-free region, which might limit PUUV persistence and therefore, the risk of NE.

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