Evidence map›Paper›PMID 42108436›Full record

ArticleBMC microbiology2026

llluminating the live-cell dynamics of early interactions between neutrophils and the microsporidian parasite Encephalitozoon cuniculi.

Eugénie Carriere, Enzo Julien, Juliette Gilbert, Julien Verlaguet, Marjolaine Vareille-Delarbre, Frédéric Delbac, Pascale Gueirard

Abstract read
In one paragraph

Article in BMC microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Eugénie CarriereCNRS UMR 6023, Laboratoire Microorganismes : Génome et environnement, Université Clermont Auvergne, Clermont-Ferrand, F-63000, France.
Enzo JulienCNRS UMR 6023, Laboratoire Microorganismes : Génome et environnement, Université Clermont Auvergne, Clermont-Ferrand, F-63000, France.
Juliette GilbertCNRS UMR 6023, Laboratoire Microorganismes : Génome et environnement, Université Clermont Auvergne, Clermont-Ferrand, F-63000, France.
Julien VerlaguetCNRS UMR 6023, Laboratoire Microorganismes : Génome et environnement, Université Clermont Auvergne, Clermont-Ferrand, F-63000, France.
Marjolaine Vareille-DelarbreCNRS UMR 6023, Laboratoire Microorganismes : Génome et environnement, Université Clermont Auvergne, Clermont-Ferrand, F-63000, France.
Frédéric DelbacCNRS UMR 6023, Laboratoire Microorganismes : Génome et environnement, Université Clermont Auvergne, Clermont-Ferrand, F-63000, France.
Pascale GueirardCNRS UMR 6023, Laboratoire Microorganismes : Génome et environnement, Université Clermont Auvergne, Clermont-Ferrand, F-63000, France. pascale.gueirard@uca.fr.

Funding

Agence Nationale de la Recherche HACKERS ANR-24-CE15-0690
6 · The paper itself

Abstract

backgroundEncephalitozoon cuniculi is an obligate intracellular parasite that affects birds and mammals, including humans, and belongs to the phylum Microsporidia. The innate immune system serves as the first line of defense against infection, but it only partially clears the parasite. Microsporidia are known to modulate the effector functions of phagocytes. They can survive and multiply inside macrophages (MOs) to evade destruction after phagocytosis and also modify the functional properties of dendritic cells. However, the role of neutrophils (PMNs) in microsporidiosis remains poorly understood. In a mouse ear skin model, inflammatory cells, including MOs and PMNs, were rapidly recruited to the cutaneous injection site, and intact spores persisted within phagocytes for several days. We hypothesized that Microsporidia also manipulate the antimicrobial mechanisms of PMNs, including phagocytosis and the formation of neutrophil extracellular traps (NETs), to enhance their survival.

resultsUsing live and static cell imaging in vitro, along with the mouse ear pinna model, we investigated the dynamics of interactions between PMNs and E. cuniculi parasites. Our observations revealed that the parasites rapidly adhere to and are phagocytosed by PMNs. After activation, infected PMNs exhibited modified structural and functional properties, such as the extension of pseudopodia, parasite lysis inside phagolysosomes, modified motility and shape parameters, and NETs formation. Interestingly, a small proportion of the parasites survived intracellularly, with early developmental stages (meronts, sporonts) observed within PMNs at 24 and 48 h post-infection. Importantly, infected PMNs harboring intact and infectious intracellular spores were later phagocytosed by MOs.

conclusionUsing innovative microscopy and imaging approaches, we discovered that E. cuniculi Microsporidia manipulate PMNs, key innate immune cells, by using them as intracellular niches for their development, and as potential vehicles for their silent transfer to other host target cells.

Indexed as

Encephalitozoon cuniculiEncephalitozoonosisNeutrophilsAnimalsExtracellular TrapsFemaleMacrophagesMicePhagocytosisSpores, FungalInnate immunityLive-cell imagingMicrosporidiaMurine modelPolymorphonuclear leukocyte

Identifiers

PMID42108436
PMCPMC13330375

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.