This study was designed to explore the impact of Lycium barbarum polysaccharide (LBP) on inflammation and gut microbiota in mice with allergic asthma. Mice were divided into four groups: control group, OVA (ovalbumin) group, Con+LBP group, OVA+LBP group. After 28 days of LBP intervention, mice were euthanized and associated indications were investigated. Histopathological examination demonstrated that LBP reduced lung injury. The results of our current study provide evidence that supplementation with LBP in asthmatic mice decreases TNF , IL-4 , IL-6 , MCP-1 , and IL-17A in plasma and bronchoalveolar lavage fluid (BALF). Sequencing and analysis of gut microbiota indicated that compared with the OVA group, Lactobacillus and Bifidobacterium were increased, but Firmicutes , Actinobacteria , Alistipes , and Clostridiales were decreased in the OVA+LBP group. We also found that gut microbiota were related to inflammation-related factors. Therefore, we speculate that LBP may improve allergic asthma by altering gut microbiota and inhibiting inflammation in mice.

Cystic echinococcosis is a chronic and complex zoonotic disease. The mechanisms underlying the parasite's establishment, growth and persistence are not completely understood, and are thought be modulated by a crosstalk through extracellular vesicles. Here, EVs were isolated from the hydatid cyst fluid of patients with cystic echinococcosis and protoscolex culture supernatant. Proteomic analysis of these EVs revealed several parasite- and human-derived proteins. Very few studies have performed proteomic analysis of EVs isolated from HCF and PCS. Our proteomic analysis of the EVs derived from HCF and PCS facilitated identification of 1175 proteins, wherein 1026 and 38 proteins were exclusively identified in the EVs derived from HCF (HCF-EVs) and PCS (PCS-EVs), respectively, and 111 proteins were shared in both. The results of co-culture of PCS-EVs with murine peripheral blood mononuclear cells showed that PCS-EVs significantly regulated T lymphocyte functions in a dose-dependent manner. Collectively, our results provide valuable information on parasite survival strategies and new insights into the role of these EVs in the establishment and persistence of hydatid cysts.

The globally distributed cystic echinococcosis (CE) is caused by the larval stage of Echinococcus granulosus (E. granulosus), a cosmopolitan and zoonotic disease with potentially life-threatening complications in humans. The emerging roles for extracellular vesicles (EVs) in parasitic infection include transferring proteins and modifying host cell gene expression to modulate host immune responses. Few studies focused on the host-derived EVs and its protein profiles. We focused on the EVs from mouse infected with E. granulosus at different stages. ExoQuick kit was used for isolating EVs from mouse plasma and ExoEasy Maxi kit was used for isolating protoscolex culture supernatant (PCS) and hydatid cyst fluid (HCF). Firstly, EVs were characterized by transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA) and immunoblot. Secondly, the proteins of plasma EVs were identified using liquid chromatography-tandem mass spectrometry (LC–MS/MS). The resulting LC–MS/MS data were processed using Maxquant search engine (v 1.5.2.8). Tandem mass spectra were researched against the mice and E. granulosus proteins database in the NCBI. The differentially expressed proteins are performed by proteomic label-free quantitative analysis and bioinformatics. Thirdly, in vitro experiment, the results of co-culture of plasma EVs and spleen mononuclear cells showed that 7W-EVs can increase the relative abundance of regulatory T (Treg) cells and IL-10. We further verified that EVs can be internalized by CD4⁺ and CD8⁺ T cells, B cells, and myeloid-derived suppressor cells (MDSC). These results implied host-derived EVs are multidirectional immune modulators. The findings can contribute to a better understanding of the role of host-derived EVs which are the optimal vehicle to transfer important cargo into host immune system. In addition, we have found several important proteins associated with E. granulosus and identified in infected mouse plasma at different stages. Furthermore, our study further highlighted the proteomics and immunological function of EVs from mouse infected with E. granulosus protoscoleces at different infection stages. We have laid a solid foundation for the role of EVs in cystic echinococcosis in the future research and supplemented a unique dataset for this E. granulosus.

Cystic echinococcosis (CE) is a common zoonotic parasitic disease that seriously impacts public health. However, the full spectrum of immune cell changes in Echinococcus granulosus infection, especially the negative immune regulation of subpopulations of regulatory T (Treg) cells, are not yet well understood.

Cystic echinococcosis (CE), a zoonotic disease caused by Echinococcus granulosus at the larval stage, predominantly develops in the liver and lungs of intermediate hosts and eventually results in organ malfunction or even death. The interaction between E. granulosus and human body is incompletely understood. Exosomes are nanosized particles ubiquitously present in human body fluids. Exosomes carry biomolecules that facilitate communication between cells. To the best of our knowledge, the role of exosomes in patients with CE is not reported. Here, we isolated exosomes from the sera of patients with CE (CE-exo) and healthy donors and subjected them to liquid chromatography-tandem mass spectrometry analysis. Proteomic analysis identified 49 proteins specifically expressed in CE-exo, including 4 proteins of parasitic origin. The most valuable parasitic proteins included tubulin alpha-1C chain and histone H4. And 8 proteins were differentially regulated in CE-exo (fold change>1.5), as analyzed with bioinformatic methods such as annotation and functional enrichment analyses. These findings may improve our understanding about the interaction between E. granulosus and human body, and may contribute to the diagnosis and prevention of CE.

The prevalence of allergic airway inflammation (AAI) worldwide is high. Artemisia annua L. pollen is spread worldwide, and allergic diseases caused by its plant polysaccharides, which are closely related to the intestinal microbiota, have anti-inflammatory effects. Further isolation and purification of Lycium barbarum L. yielded its most effective component Lycium barbarum L. glycopeptide (LbGP), which can inhibit inflammation in animal models. However, its therapeutic effect on AAI and its mechanism of regulating the intestinal flora have not been fully investigated. To explore LbGP in APE-induced immunological mechanisms of AAI and the interaction mechanism of the intestinal flora and metabolites. A mouse model of AAI generated from Artemisia annua pollen was constructed, and immunological indices related to the disease were examined. A combination of macrogenomic and metabolomic analyses was used to investigate the effects of LbGP on the gut microbial and metabolite profiles of mice with airway inflammation. LbGP effectively alleviated Artemisia. annua pollen extract (APE)-induced AAI, corrected Th1/Th2 immune dysregulation, decreased Th17 cells, increased Treg cells, and altered the composition and function of the intestinal microbiota. LbGP treatment increased the number of OdoribacterandDuncaniella in the intestines of the mice, but the numble of Alistipes and Ruminococcus decreased. Metabolite pathway enrichment analysis were used to determine the effects of taurine and hypotaurine metabolism, bile acid secretion, and pyrimidine metabolism pathways on disease. Our results revealed significant changes in the macrogenome and metabolome following APE and LbGP intervention, revealed potential correlations between gut microbial species and metabolites, and highlighted the beneficial effects of LbGP on AAI through the modulation of the gut microbiome and host metabolism.