Macrophage-mediated mechanisms of lung injury in the sensitization reaction to Echinococcus granulosus.

Objective: In this study, the impact of inhibiting the PI3K/AKT/NF-κB pathway on lung oxidative damage induced by Echinococcus granulosus cyst fluid was investigated. Methods: Twenty-four mice were randomly assigned to four groups. Three months after inoculation with hydatid cyst segments, mice in group A were treated with intraperitoneal and intratracheal saline injections; mice in group B were administered a caudal vein injection of a PI3K inhibitor, followed by cyst fluid sensitization; mice in group C received an AKT inhibitor via caudal vein, followed by cyst fluid sensitization; and mice in group D were subjected to cyst fluid sensitization without any inhibitor treatment. Cellular changes in lung tissues across all groups were evaluated, including pathological section analysis. Analysis of pulmonary tissue and serum from these mice included the assessment of PI3K/AKT/NF-κB pathway proteins, inflammatory factors, and related mRNA levels. Results: Mice in groups B and C exhibited a higher proportion of M2-type macrophages and significantly lower levels of PI3K/AKT/NF-κB pathway proteins, inflammatory factors (interleukin-6 [IL-6]/tumor necrosis factor-α [TNF-α]), and oxidative markers in lung tissues compared to mice in group D (P < 0.05). Conclusion: Our results in this study indicate that activation of the PI3K/AKT/NF-κB pathway contributed to an increase in the M1 macrophage phenotype, leading to enhanced secretion of peroxidases and inflammatory factors. This mechanism plays a crucial role in the oxidative and inflammatory lung damage associated with allergic reactions to E. granulosus cyst fluid.

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.