The role of memory T cells in Echinococcus granulosus-induced sensitization.

OBJECTIVE: To investigate the changes in memory T cells and the related factors in mice by the establishment of a BALB/c mouse model of Echinococcus granulosus-induced sensitization. METHODS: A sensitized BALB/c mouse model was established by intraperitoneal injection of E. granulosus. A control group (CTRL), a nonsensitized group infected with E. granulosus (CE), and a sensitized group infected with E. granulosus (ANPC) were set up. The pathological changes in lung tissue in mice, the change in memory T cells (CD4 Tm), and the change in peripheral blood nucleated interleukin-23 (IL-23) were detected using HE staining, flow cytometry, and liquid-phase multiple protein quantification techniques, respectively. RESULTS: The individual percentage of mouse memory T cells was 9.14 ± 0.45, 25.23 ± 0.17, and 13.29 ± 0.32 in the CTRL, CE, and ANPC groups, respectively. The percentage of memory T cells in the ANPC group was higher than that in the CTRL group (t = 18.410, p < .001) but lower than that in the CE group (t = -80.147, p < .001). The levels of IL-23 in peripheral blood of mice in the CTRL, CE, and ANPC groups were 225.76 ± 27.16, 359.21 ± 28.67, and 215.69 ± 22.69, respectively. The level of IL-23 in peripheral blood of mice in the ANPC group was lower than that in the CE group (t = 9.609, p < .001), and there was no statistical difference with the CTRL group (t = 0.697, p = .502). CONCLUSION: In the BALB/c mouse model of E. granulosus-induced sensitization, the expression of IL-23 in peripheral blood increased, and the memory T cell proliferated and became activated; there was a decrease in the content of IL-23 in peripheral blood and number of activated memory T cells in the sensitization group infected with E. granulosus. The E. granulosus-induced allergic reaction was related to IL-23 and the activation of memory T cells.

The regulatory role of differential microRNA expressions on cellular inflammatory factors IL-6 and IL-10 in Echinococcus granulosus-induced anaphylaxis.

OBJECTIVE: To determine the pathogenesis and molecular targets of anaphylaxis caused by hydatid cyst fluid leakage. METHODS: First, Balb/c mice were infected with Echinococcus granulosus, and then the anaphylaxis model was developed. The mice were separated into: anaphylaxis caused by the cystic echinococcosis group (ANPC), the cystic echinococcosis without anaphylaxis group (CE group), and the normal control group (CTRL). Following this, the spleen tissue was collected for microRNA (miRNA) sequencing. Using bioinformatics analysis, differentially expressed miRNAs (DEMs) were identified. Then, through the use of protein-protein interaction (PPI) networks, the key target genes for miRNA regulation associated with echinococcosis-induced anaphylaxis were identified. RESULTS: ANPC and CE groups have 29 and 39 DEMs compared to the CTRL group, respectively. Based on these 25 DEMs, interactions between miRNA and mRNA were screened, and 174 potential target genes were identified. We performed gene ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis on these 174 target genes, and the results revealed that the three pathways with the highest enrichment were the PI3K-Akt signaling pathway, FoxO signaling pathway, and Focal adhesion. The interaction analysis of PPI and miRNA-hub gene networks revealed that interleukin 6 (IL-6) was regulated by miR-146a-5p and miR-149-5p, while IL-10 was regulated by miR-29b-3p and miR-29c-3. Using reverse transcription polymerase chain reaction, we found that the miRNAs regulating IL-6 and IL-10 were significantly upregulated in the ANPC group, and there are three pathways involved in that process: Pathways of PI3K-Akt signaling, FoxO signaling, and Focal adhesion. IL-6 and IL-10 play an important role in cellular pyroptosis and apoptosis. Therefore, the aforementioned results provide significant reference value for elucidating the mechanism of cellular pyroptosis and apoptosis in echinococcosis-induced anaphylaxis, and for formulating tissue and organ protection strategies for patients with cystic echinococcosis when anaphylaxis is triggered by hydatid cyst rupture.