Xiao He
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Xiao He has a total of 6 co-authors. Here are the top co-authors by number of shared publications:
- Biying Mo
State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400715, China
1 shared publication - Guozhen An
Sate Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400715, China
1 shared publication - Jialing Bao
The State Key Laboratory of Resource Insects, Southwest University
1 shared publication - Maoshuang Ran
State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400715, China
1 shared publication - Yunlin Tang
State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400715, China
1 shared publication - Zeyang Zhou
State Key Laboratory of Resource Insects, Southwest University
1 shared publication
Latest Publications
- Open Access
- 29 November 2020
- Published by MDPI AG in Microorganisms
- Vol. 8 (12) , 1891
Characterization of a Murine Model for Encephalitozoon hellem Infection after Dexamethasone Immunosuppression
Background: Encephalitozoon hellem (E. hellem) belongs to a group of opportunistic pathogens called microsporidia. Microsporidia infection symptoms vary and include diarrhea, ocular disorders and systemic inflammations. Traditionally, immunodeficient animals were used to study microsporidia infection. To overcome the difficulties in maintenance and operation using immunodeficient mice, and to better mimic natural occurring microsporidia infection, this study aims to develop a pharmacologically immunosuppressed murine model of E. hellem infection. Methods: Wild-type C57BL/6 mice were immunosuppressed with dexamethasone (Dex) and then E. hellem spores were inoculated into the mice intraperitoneally. Control groups were the Dex-immunosuppressed but noninoculated mice, and the Dex-immunosuppressed then lipopolysaccharide (LPS)-treated mice. Mice body weights were monitored and all animals were sacrificed at the 15th day after inoculation. Tissue fragments and immune cells were collected and processed. Results: Histopathological analysis demonstrated that E. hellem inoculation resulted in a disseminated nonlethal infection. Interestingly, E. hellem infection desensitized the innate immunity of the host, as shown by cytokine expressions and dendritic cell maturation. We also found that E. hellem infection greatly altered the composition of host gut microbiota. Conclusions: Dex-immunosuppressed mice provide a useful tool for study microsporidiosis and the interactions between microsporidia and host immunity.
- 29 November 2020
- Published by MDPI AG in Microorganisms
- Vol. 8 (12) , 1891
Open AccessCharacterization of a Murine Model for Encephalitozoon hellem Infection after Dexamethasone Immunosuppression
Background: Encephalitozoon hellem (E. hellem) belongs to a group of opportunistic pathogens called microsporidia. Microsporidia infection symptoms vary and include diarrhea, ocular disorders and systemic inflammations. Traditionally, immunodeficient animals were used to study microsporidia infection. To overcome the difficulties in maintenance and operation using immunodeficient mice, and to better mimic natural occurring microsporidia infection, this study aims to develop a pharmacologically immunosuppressed murine model of E. hellem infection. Methods: Wild-type C57BL/6 mice were immunosuppressed with dexamethasone (Dex) and then E. hellem spores were inoculated into the mice intraperitoneally. Control groups were the Dex-immunosuppressed but noninoculated mice, and the Dex-immunosuppressed then lipopolysaccharide (LPS)-treated mice. Mice body weights were monitored and all animals were sacrificed at the 15th day after inoculation. Tissue fragments and immune cells were collected and processed. Results: Histopathological analysis demonstrated that E. hellem inoculation resulted in a disseminated nonlethal infection. Interestingly, E. hellem infection desensitized the innate immunity of the host, as shown by cytokine expressions and dendritic cell maturation. We also found that E. hellem infection greatly altered the composition of host gut microbiota. Conclusions: Dex-immunosuppressed mice provide a useful tool for study microsporidiosis and the interactions between microsporidia and host immunity.