Preliminary expression profile of cytokines in brain tissue of BALB/c mice with Angiostrongylus cantonensis infection

Abstract

BackgroundAngiostrongylus cantonensis (A. cantonensis) infection can result in increased risk of eosinophilic meningitis. Accumulation of eosinophils and inflammation can result in the A. cantonensis infection playing an important role in brain tissue injury during this pathological process. However, underlying mechanisms regarding the transcriptomic responses during brain tissue injury caused by A. cantonensis infection are yet to be elucidated. This study is aimed at identifying some genomic and transcriptomic factors influencing the accumulation of eosinophils and inflammation in the mouse brain infected with A. cantonensis.MethodsAn infected mouse model was prepared based on our laboratory experimental process, and then the mouse brain RNA Libraries were constructed for deep Sequencing with Illumina Genome Analyzer. The raw data was processed with a bioinformatics’ pipeline including Refseq genes expression analysis using cufflinks, annotation and classification of RNAs, lncRNA prediction as well as analysis of co-expression network. The analysis of Refseq data provides the measure of the presence and prevalence of transcripts from known and previously unknown genes.ResultsThis study showed that Cys-Cys (CC) type chemokines such as CCL2, CCL8, CCL1, CCL24, CCL11, CCL7, CCL12 and CCL5 were elevated significantly at the late phase of infection. The up-regulation of CCL2 indicated that the worm of A. cantonensis had migrated into the mouse brain at an early infection phase. CCL2 could be induced in the brain injury during migration and CCL2 might play a major role in the neuropathic pain caused by A. cantonensis infection. The up-regulated expression of IL-4, IL-5, IL-10, and IL-13 showed Th2 cell predominance in immunopathological reactions at late infection phase in response to infection by A. cantonensis. These different cytokines can modulate and inhibit each other and function as a network with the specific potential to drive brain eosinophilic inflammation. The increase of ATF-3 expression at 21 dpi suggested the injury of neuronal cells at late phase of infection. 1217 new potential lncRNA were candidates of interest for further research.ConclusionsThese cytokine networks play an important role in the development of central nervous system inflammation caused by A. cantonensis infection.Electronic supplementary materialThe online version of this article (doi:10.1186/s13071-015-0939-6) contains supplementary material, which is available to authorized users.

Neuronal Apoptosis: Pathological Basis of Behavioral Dysfunctions Induced by Angiostrongylus cantonensis in Rodents Model

“…Similarly, the samples from the control mice were collected on the 21st day PI, and the samples were frozen in liquid nitrogen. The overall flow of RNA library construction and deep sequencing had been shown in our previous study [ 36 ].…”

Stimulation of IL-1β and IL-6 through NF-κB and sonic hedgehog-dependent pathways in mouse astrocytes by excretory/secretory products of fifth-stage larval Angiostrongylus cantonensis

“…By 2010, more than 3000 cases had been reported in approximately 30 countries worldwide [ 29 , 30 ]. In A. cantonensis infection, the fifth-stage larvae (L5) induce a wide range of immune responses, including eosinophil recruitment and cytokine release (IL-1β, IL-4, IL-5, IL-6, IL-10, IL-13 and TNF-α) in the CNS of humans [ 31 , 32 ].…”

Initial events in the breakthrough of the epithelial barrier of the small intestine by Angiostrongylus cantonensis

“…However, unlike the fact that A. costaricensis lived inside intestinal small vessels, A. cantonensis had no direct contact with the colon in its life cycle. These symptoms of eosinophilic infiltration in the colon might be related to host interleukin and eosinophil responses [30,31], but not to larval invasion.…”