Comparative proteomics reveals Cryptosporidium parvum infection disrupts cellular barriers

Wang, Luyang; Cui, Zhaohui; Li, Na; Liang, Guanda; Zhang, Xiaotian; Wang, Yuexin; Li, Dongfang; Li, Xiaoying; Zhang, Longxian

doi:10.1016/j.jprot.2023.104969

Cited by 2 publications

(3 citation statements)

References 41 publications

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“…Previous studies have also confirmed that host innate immunity plays a significant role in the course of C. parvum infection [26]. In this study, KEGG analysis of the transcriptomes showed that the cell adhesion pathway was the second significantly upregulated in mice during C. parvum IId infection, which also seen in C. parvum infected HCT-8 cells [24,27]. There were some cases that excessive inflammatory response could result the host's diarrheal death [28], and cell adhesion molecules were involved in regulating cell migration and apoptosis [29].…”

Section: Discussionsupporting

confidence: 71%

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Cryptosporidium parvum disrupts intestinal epithelial barrier in neonatal mice through downregulation of cell junction molecules

Luo,

Xu,

Zhang

et al. 2024

PLoS Negl Trop Dis

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Background Cryptosporidium spp. cause watery diarrhea in humans and animals, especially in infants and neonates. They parasitize the apical surface of the epithelial cells in the intestinal lumen. However, the pathogenesis of Cryptosporidium-induced diarrhea is not fully understood yet. Methodology/principal findings In this study, we infected C57BL/6j neonatal mice with C. parvum IIa and IId subtypes, and examined oocyst burden, pathological changes, and intestinal epithelial permeability during the infection. In addition, transcriptomic analyses were used to study the mechanism of diarrhea induced by the C. parvum IId subtype. The neonatal mice were sensitive to both C. parvum IIa and IId infection, but the IId subtype caused a wide oocyst shedding window and maintained the high oocyst burden in the mice compared with the IIa subtype. In addition, the mice infected with C. parvum IId resulted in severe intestinal damage at the peak of infection, leading to increased permeability of the epithelial barrier. The KEGG, GO and GSEA analyses revealed that the downregulation of adherens junction and cell junction molecules at 11 dpi. Meanwhile, E-cadherin, which is associated with adherens junction, was reduced at the protein level in mouse ileum at peak and late infection. Conclusions/significance C. parvum IId infection causes more severe pathological damage than C. parvum IIa infection in neonatal mice. Furthermore, the impairment of the epithelial barrier during C. parvum IId infection results from the downregulation of intestinal junction proteins.

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Section: Discussionsupporting

confidence: 71%

“…parvum IId infection, which also seen in C . parvum infected HCT-8 cells [ 24 , 27 ]. There were some cases that excessive inflammatory response could result the host’s diarrheal death [ 28 ], and cell adhesion molecules were involved in regulating cell migration and apoptosis [ 29 ].…”

Section: Discussionmentioning

confidence: 99%

Cryptosporidium parvum disrupts intestinal epithelial barrier in neonatal mice through downregulation of cell junction molecules

Luo,

Xu,

Zhang

et al. 2024

PLoS Negl Trop Dis

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“…To predict subcellular localization, the amino acid sequences of target proteins are obtained from the UniProt database, and these sequences are then inputted into the PSORT II online software (https://psort.hgc.jp/, accessed on 21 July 2023). PSORT II provides predictions regarding the subcellular location of these target proteins [21].…”

Section: Protein Subcellular Localizationmentioning

confidence: 99%

Structure–Activity Relationship Target Prediction Studies of Clindamycin Derivatives with Broad-Spectrum Bacteriostatic Antibacterial Properties

Jia,

Zhang,

Zhu

2023

Molecules

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This study investigated the potential of clindamycin derivatives with broad-spectrum antibacterial properties. The main goal was to identify new antibacterial targets to lay the foundation for developing novel antimicrobial agents. This research used molecular docking and dynamics simulations to explore how clindamycin derivatives could combat bacterial resistance and widen their antibacterial capabilities. Three different clindamycin derivatives were studied against 300 target proteins. Among these, 26 proteins were found to be common targets for all three derivatives. After further screening through molecular docking and dynamics simulations, four specific protein targets were identified. Notably, one of these targets, cell division protein FtsZ, was found to be primarily located in the cyto and cyto_nucl compartments. These findings suggest that clindamycin derivatives have the potential to address bacterial resistance and broaden their antibacterial effectiveness through these identified protein targets.

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Comparative proteomics reveals Cryptosporidium parvum infection disrupts cellular barriers

Cited by 2 publications

References 41 publications

Cryptosporidium parvum disrupts intestinal epithelial barrier in neonatal mice through downregulation of cell junction molecules

Cryptosporidium parvum disrupts intestinal epithelial barrier in neonatal mice through downregulation of cell junction molecules

Structure–Activity Relationship Target Prediction Studies of Clindamycin Derivatives with Broad-Spectrum Bacteriostatic Antibacterial Properties

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