Genetic Influence on Frequencies of Myeloid-Derived Cell Subpopulations in Mouse

Krayem, Imtissal; Sohrabi, Yahya; Javorková, Eliška; Volkova, Valeriya; Strnad, Hynek; Havelková, Helena; Vojtíšková, Jarmila; Aidarova, Aigerim; Holáň, Vladimı́r; Démant, Peter; Lipoldová, Marie

doi:10.3389/fimmu.2021.760881

Cited by 4 publications

(3 citation statements)

References 83 publications

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“…Krayem et al [ 30 ] identified a unique mouse strain, B10.O20, in the spleen, which showed a significantly higher frequency of myeloid-derived cells, such as CD11b + , CD11b + Gr1 + , CD14 + , and F4/80 + cells than other strains of mice. In that study, a bioinformatics analysis of genomic sequences indicated that Rab44 was a candidate gene for influencing the frequencies of immune cell subpopulations, since the mouse strain displayed different expression levels of Rab44 mRNA and a Rab44 gene mutation G275R, in which glycine at the position of the Rab44 gene was changed to arginine [ 30 ]. Therefore, it is likely that the Rab44 expression levels are involved in frequencies of immune-cell subpopulations in mice.…”

Section: Discussionmentioning

confidence: 99%

Rab44 Deficiency Induces Impaired Immune Responses to Nickel Allergy

Noguromi

Yamaguchi²,

Satô³

et al. 2023

IJMS

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Rab44 was recently identified as an atypical Rab GTPase that possesses EF-hand and coiled-coil domains at the N-terminus, and a Rab-GTPase domain at the C-terminus. Rab44 is highly expressed in immune-related cells such as mast cells, macrophages, osteoclasts, and granulocyte-lineage cells in the bone marrow. Therefore, it is speculated that Rab44 is involved in the inflammation and differentiation of immune cells. However, little is known about the role of Rab44 in inflammation. In this study, we showed that Rab44 was upregulated during the early phase of differentiation of M1- and M2-type macrophages. Rab44-deficient mice exhibited impaired tumor necrosis factor alpha and interleukin-10 production after lipopolysaccharide (LPS) stimulation. The number of granulocytes in Rab44-deficient mice was lower, but the lymphocyte count in Rab44-deficient mice was significantly higher than that in wild-type mice after LPS stimulation. Moreover, Rab44-deficient macrophages showed impaired nickel-induced toxicity, and Rab44-deficient mice showed impaired nickel-induced hypersensitivity. Upon nickel hypersensitivity induction, Rab44-deficient mice showed different frequencies of immune cells in the blood and ears. Thus, it is likely that Rab44 is implicated in immune cell differentiation and inflammation, and Rab44 deficiency induces impaired immune responses to nickel allergies.

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Section: Discussionmentioning

confidence: 99%

Rab44 Deficiency Induces Impaired Immune Responses to Nickel Allergy

Noguromi

Yamaguchi²,

Satô³

et al. 2023

IJMS

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“…We have sequenced the genomes of the strains BALB/c and STS using the next-generation sequencing (NGS) system HiSeq 2500 (Illumina, California, United States) (12× coverage) and analyzed them as described in (49,50). In detail, NGS data were preprocessed using the software Trimmomatic (51), and overlapping pair reads were joined by the software Flash (52).…”

Section: Detection Of Polymorphisms That Change Rna Stability and The...mentioning

confidence: 99%

Functionally distinct regions of the locus Leishmania major response 15 control IgE or IFNγ level in addition to skin lesions

et al. 2023

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Leishmaniasis, a disease caused by parasites of Leishmania spp., endangers more than 1 billion people living in endemic countries and has three clinical forms: cutaneous, mucocutaneous, and visceral. Understanding of individual differences in susceptibility to infection and heterogeneity of its pathology is largely lacking. Different mouse strains show a broad and heterogeneous range of disease manifestations such as skin lesions, splenomegaly, hepatomegaly, and increased serum levels of immunoglobulin E and several cytokines. Genome-wide mapping of these strain differences detected more than 30 quantitative trait loci (QTLs) that control the response to Leishmania major. Some control different combinations of disease manifestations, but the nature of this heterogeneity is not yet clear. In this study, we analyzed the L. major response locus Lmr15 originally mapped in the strain CcS-9 which carries 12.5% of the genome of the resistant strain STS on the genetic background of the susceptible strain BALB/c. For this analysis, we used the advanced intercross line K3FV between the strains BALB/c and STS. We confirmed the previously detected loci Lmr15, Lmr18, Lmr24, and Lmr27 and performed genetic dissection of the effects of Lmr15 on chromosome 11. We prepared the interval-specific recombinant strains 6232HS1 and 6229FUD, carrying two STS-derived segments comprising the peak linkage of Lmr15 whose lengths were 6.32 and 17.4 Mbp, respectively, and analyzed their response to L. major infection. These experiments revealed at least two linked but functionally distinct chromosomal regions controlling IFNγ response and IgE response, respectively, in addition to the control of skin lesions. Bioinformatics and expression analysis identified the potential candidate gene Top3a. This finding further clarifies the genetic organization of factors relevant to understanding the differences in the individual risk of disease.

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“…Each CcS/Dem strain contains a different, random set of approximately 12.5% genes of the donor strain STS and approximately 87.5% genes of the background strain BALB/c (Demant and Hart 1986 ; Stassen et al 1996 ). B10.O20 carries 3.6% of genes of the strain O20 on the B10 genetic background (Krayem et al 2022 ). Strains were classified as resistant or susceptible according to their organ pathology and parasite load in organs (Lipoldová et al 2002 ; Sohrabi et al 2018 ).…”

Section: Introductionmentioning

confidence: 99%

Effects of Leishmania major infection on the gut microbiome of resistant and susceptible mice

Mrázek,

Mrázková,

Mekadim

et al. 2024

Appl Microbiol Biotechnol

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Cutaneous leishmaniasis, a parasitic disease caused by Leishmania major, is a widely frequent form in humans. To explore the importance of the host gut microbiota and to investigate its changes during L. major infection, two different groups of mouse models were assessed. The microbiome of two parts of the host gut—ileum and colon—from infected and non-infected mice were characterised by sequencing of 16S rDNA using an Ion Torrent PGM platform. Microbiome analysis was performed to reveal changes related to the susceptibility and the genetics of mice strains in two different gut compartments and to compare the results between infected and non-infected mice. The results showed that Leishmania infection affects mainly the ileum microbiota, whereas the colon bacterial community was more stable. Different biomarkers were determined in the gut microbiota of infected resistant mice and infected susceptible mice using LEfSe analysis. Lactobacillaceae was associated with resistance in the colon microbiota of all resistant mice strains infected with L. major. Genes related to xenobiotic biodegradation and metabolism and amino acid metabolism were primarily enriched in the small intestine microbiome of resistant strains, while genes associated with carbohydrate metabolism and glycan biosynthesis and metabolism were most abundant in the gut microbiome of the infected susceptible mice. These results should improve our understanding of host-parasite interaction and provide important insights into the effect of leishmaniasis on the gut microbiota. Also, this study highlights the role of host genetic variation in shaping the diversity and composition of the gut microbiome. Key points • Leishmaniasis may affect mainly the ileum microbiota while colon microbiota was more stable. • Biomarkers related with resistance or susceptibility were determined in the gut microbiota of mice. • Several pathways were predicted to be upregulated in the gut microbiota of resistant or susceptible mice. Graphical Abstract

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Genetic Influence on Frequencies of Myeloid-Derived Cell Subpopulations in Mouse

Cited by 4 publications

References 83 publications

Rab44 Deficiency Induces Impaired Immune Responses to Nickel Allergy

Rab44 Deficiency Induces Impaired Immune Responses to Nickel Allergy

Functionally distinct regions of the locus Leishmania major response 15 control IgE or IFNγ level in addition to skin lesions

Effects of Leishmania major infection on the gut microbiome of resistant and susceptible mice

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