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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Microarray analysis of bone marrow derived macrophages stimulated with helminth larvae and immune serum

ABSTRACT: Mouse bone marrow derived macrophages were stimulated with L3 larvae of the helminth Heligmosomoides polygyrus (Hp) (500 L3 /1 mio cells) in the presence or absence of immune serum (1:50 v:v) from challenge-Hp-infected mice.

ORGANISM(S): Mus musculus

SUBMITTER: Julia Esser-von Bieren

PROVIDER: E-MEXP-3920 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The production of Excretory-Secretory molecules from Heligmosomoides polygyrus bakeri fourth stage larvae varies between mixed and single sex cultures.

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2021-09-10 | PXD023759 | Pride

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Exosomes secreted by a nematode parasite transfer small RNAs to mammalian cells and regulate genes of the innate immune system [Heligmosomoides polygyrus]

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Genome-wide expression analysis of the effects of a parasitic nematode's secreted exosomes on mammalian cells.

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Heligmosomoides polygyrus

Project description:Heligmosomoides polygyrus overview

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Exosomes secreted by a nematode parasite transfer small RNAs to mammalian cells and regulate genes of the innate immune system [Litomosoides sigmodontis]

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Intestinal tissues (duodenum) from wild-type (BALB/c) and MIF deficient mice were compared in the steady state and at two different time points (day 3 and day 7) following infection with the gastrointestinal helminth parasite Heligmosomoides polygyrus

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Epithelial-Cell-Derived Phospholipase A2 Group 1B Is an Endogenous Anthelmintic

Project description:Immunity to intestinal helminth infections has been well studied, but the mechanism of helminth killing prior to expulsion remains unclear. Here we identify epithelial-cell-derived phospholipase A2 group 1B (PLA2g1B) as a host-derived endogenous anthelmintic. PLA2g1B is elevated in resistant mice and is responsible for killing tissue-embedded larvae. Despite comparable activities of other essential type-2-dependent immune mechanisms, Pla2g1b-/- mice failed to expel the intestinal helminths Heligmosomoides polygyrus or Nippostrongylus brasiliensis. Expression of Pla2g1b by epithelial cells was dependent upon intestinal microbiota, adaptive immunity, and common-gamma chain-dependent signaling. Notably, Pla2g1b was downregulated in susceptible mice and inhibited by IL-4R-signaling in vitro, uncoupling parasite killing from expulsion mechanisms. Resistance was restored in Pla2g1b-/- mice by treating infective H. polygyrus L3 larvae with PLA2g1B, which reduced larval phospholipid abundance. These findings uncover epithelial-cell-derived Pla2g1b as an essential mediator of helminth killing, highlighting a previously overlooked mechanism of anti-helminth immunity.

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