Abstract
AbstractSpecies ofEimeria(Apicomplexa:Coccidia) differ in the timing of lifecycle progression and resulting infections vary in host immune reactions and pathology they induce.Eimeriainfections in house mice are used as models for basic immunology and the most commonly used isolates have been passaged in laboratory mice for over 50 years. We questioned in how far such isolates are still representative for infections in natural systems.In the current study, we address this question by comparing the “laboratory isolate”E. falciformisBayerHaberkorn1970 with a novel, wild derived isolateE. falciformisBrandenburg88, and contrast this with another novel wild derived isolate,E. ferrisiBrandenburg64. We compare parasite lifecycle progression. We relate this to immune cell infiltration at the site of infection (in the caecum) and cytokine gene expression in the spleen as a measure of host immune response. We assess host weight loss as a measure of pathogenicity.A species-specific slower parasite lifecyle progression and higher pathogenicity are observed forE. falciformis vs. E. ferrisi.Host cytokines, in contrast, are expressed at significantly higher level in the spleen of mice infected with theE. falciformislaboratory isolate than in both wild derived isolates, irrespective of the species. Differences in histopathology are observable between all three isolates: TheE. falciformisBayerHaberkorn1970 laboratory isolate induces the strongest inflammation and cellular infiltration (with lymphocytes, plasma cells and eosinophilic granulocytes) followed by the wild derivedE. falciformisBrandenburg88 isolate.E. ferrisiBrandenburg64 is inducing milder histological changes than bothE. falciformisisolates.It can be speculated that the serial passaging ofE. falciformisBayerHaberkorn1970 has resulted in evolutionary divergence rendering this isolate more virulent in NMRI mice. Caution is needed when findings from experimental infection with laboratory strains should be integrated with observations in natural systems.HighlightsE. ferrisihas a shorter pre-patency thanwild-derived and laboratory isolates ofE. falciformis.E. ferrisiis less virulent than bothE. falciformisisolates and the timing of maximal oocyst shedding relative to host weight loss differs.The laboratory strain ofE. falciformisinduces stronger cytokine expression in the spleen than both wild derived strains ofE. falciformisandE. ferrisi.The laboratory strain ofE. falciformisinduces stronger tissue infiltration of immune cells than the wild-derived strain.E. ferrisiinfections are associated with the lowest infiltration.
Publisher
Cold Spring Harbor Laboratory
Cited by
8 articles.
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