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Updated: Mar 8, 2026

Studying Inherited Immunity in a Caenorhabditis elegans Model of Microsporidia Infection
Published on: April 6, 2022
Microsporidia infection impacts the host cell's cycle and reduces host cell apoptosis
Raquel Martín-Hernández1,2, Mariano Higes1, Soledad Sagastume1
1Laboratorio de Patología Apícola, Centro de Investigación Apícola y Agroambiental, IRIAF, Consejería de Agricultura de la Junta de Comunidades de Castilla-La Mancha, Marchamalo, Spain.
Abstract:
Intracellular parasites can alter the cellular machinery of host cells to create a safe haven for their survival. In this regard, microsporidia are obligate intracellular fungal parasites with extremely reduced genomes and hence, they are strongly dependent on their host for energy and resources. To date, there are few studies into host cell manipulation by microsporidia, most of which have focused on morphological aspects. The microsporidia Nosema apis and Nosema ceranae are worldwide parasites of honey bees, infecting their ventricular epithelial cells. In this work, quantitative gene expression and histology were studied to investigate how these two parasites manipulate their host's cells at the molecular level. Both these microsporidia provoke infection-induced regulation of genes involved in apoptosis and the cell cycle. The up-regulation of buffy (which encodes a pro-survival protein) and BIRC5 (belonging to the Inhibitor Apoptosis protein family) was observed after infection, shedding light on the pathways that these pathogens use to inhibit host cell apoptosis. Curiously, different routes related to cell cycle were modified after infection by each microsporidia. In the case of N. apis, cyclin B1, dacapo and E2F2 were up-regulated, whereas only cyclin E was up-regulated by N. ceranae, in both cases promoting the G1/S phase transition. This is the first report describing molecular pathways related to parasite-host interactions that are probably intended to ensure the parasite's survival within the cell.
Insights
Honey bee parasites Nosema apis and Nosema ceranae manipulate host cells by altering apoptosis and cell cycle genes. This molecular interaction helps the microsporidia ensure their survival within the host bee cells.
Area of Science:
- * Parasitology
- * Molecular Biology
- * Apiculture
Background:
- * Microsporidia are obligate intracellular fungal parasites dependent on host cells for survival.
- * Honey bees are globally affected by Nosema apis and Nosema ceranae, which infect ventricular epithelial cells.
- * Previous research on microsporidian host cell manipulation primarily focused on morphological changes.
Purpose of the Study:
- * To investigate the molecular mechanisms of host cell manipulation by Nosema apis and Nosema ceranae.
- * To analyze gene expression changes related to apoptosis and the cell cycle in honey bee cells post-infection.
- * To elucidate parasite-host interaction pathways at the molecular level.
Main Methods:
- * Quantitative gene expression analysis.
- * Histological examination of infected honey bee tissues.
- * Comparative analysis of molecular responses to N. apis and N. ceranae infections.
Main Results:
- * Both N. apis and N. ceranae infections induced significant gene expression changes in apoptosis and cell cycle pathways.
- * Upregulation of "buffy" and BIRC5 genes suggests inhibition of host cell apoptosis by both parasites.
- * Distinct alterations in cell cycle regulation were observed: N. apis upregulated cyclin B1, dacapo, and E2F2, while N. ceranae upregulated cyclin E, both promoting G1/S phase transition.
Conclusions:
- * Microsporidia actively manipulate host cell molecular pathways to facilitate their survival.
- * Inhibition of apoptosis and promotion of cell cycle progression are key strategies employed by Nosema species.
- * This study provides the first molecular insights into Nosema-honey bee interactions, revealing parasite-driven manipulation of host cellular processes.
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