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Updated: Sep 30, 2025
A Non-invasive and Technically Non-intensive Method for Induction and Phenotyping of Experimental Bacterial Pneumonia in Mice
Published on: September 28, 2016
Opportunistic pneumonia caused by E. cuniculi in mice immunosuppressed with cyclophosphamide
Iramirton Figuerêdo Moreira1, Anuska Marcelino Alvares-Saraiva2, Elizabeth Cristina Pérez2
1Programa de Pós-Graduação em Patologia Ambiental e Experimental, Universidade Paulista (UNIP), Rua Dr. Bacelar 902, CEP 04057-000, São Paulo, SP, Brazil; Faculdade de Medicina da Universidade Federal de Alagoas, Campus A. C. Simões Tabuleiro do Martins, CEP 57072-900, Maceió, AL, Brazil.
Abstract:
Opportunistic fungal pneumonia is a cause of concern in immunocompromised patients due to its high morbidity and mortality rates. One such opportunistic agent affecting immunocompromised patients is the microsporidia called Encephalitozoon cuniculi. This study aimed to evaluate pneumonia caused by E. cuniculi in mice treated with the immunosuppressive agent cyclophosphamide (Cy). This study also aimed to describe the immune cells associated with the microsporidial pneumonia. C57BL/6 mice were infected intravenously with E. cuniculi spores and treated with Cy (75 mg/kg/week, intraperitoneally). Thirty days post-infection, the fungal burden (qPCR), histopathological lesions, cytokine production, and the phenotype of the immune cells in the lung parenchyma were evaluated. Histologically, interstitial pneumonia with lymphocytic infiltrate was observed in the infected animals. The infiltrate mainly consisted of CD8+ and CD4+ T lymphocytes, with reduced populations of B lymphocytes and macrophages. The production of tumor necrosis factor-alpha (TNF-α) was significant in the animals of the infected groups. Also, the fungal burden was higher in the Cy-treated animals, which was confirmed by the immunohistochemical observation of spores. These results demonstrated that E. cuniculi infection of C57BL/6 mice caused lymphocytic interstitial pneumonia (characterized by a predominant lymphocytic infiltrate), which was aggravated by Cy-induced immunosuppression. Thus, these results can be used to understand the different pathological, immunological, and therapeutic aspects of lymphocytic interstitial pneumonia.
Insights
Encephalitozoon cuniculi causes lymphocytic interstitial pneumonia in mice. Immunosuppression with cyclophosphamide worsened fungal burden and lung inflammation, highlighting therapeutic targets for opportunistic infections.
Area of Science:
- Immunology
- Pathology
- Mycology
Background:
- Opportunistic fungal pneumonia poses significant risks to immunocompromised individuals.
- Microsporidia, such as Encephalitozoon cuniculi, are emerging pathogens in this population.
- Understanding the host-pathogen interactions is crucial for managing these infections.
Purpose of the Study:
- To investigate Encephalitozoon cuniculi-induced pneumonia in a mouse model.
- To assess the impact of cyclophosphamide-induced immunosuppression on the infection.
- To characterize the immune cell response during microsporidial pneumonia.
Main Methods:
- C57BL/6 mice were infected with E. cuniculi and treated with cyclophosphamide.
- Evaluated fungal burden using qPCR and immunohistochemistry.
- Assessed histopathological lesions, cytokine production (TNF-α), and immune cell phenotypes (CD8+, CD4+, B cells, macrophages) in lung tissue.
Main Results:
- E. cuniculi infection led to interstitial pneumonia with lymphocytic infiltrate.
- CD8+ and CD4+ T lymphocytes predominated in the lung infiltrate.
- Cyclophosphamide treatment increased fungal burden and exacerbated pneumonia.
- Elevated TNF-α production was observed in infected mice.
Conclusions:
- E. cuniculi infection causes lymphocytic interstitial pneumonia in mice.
- Cyclophosphamide exacerbates E. cuniculi pneumonia, increasing fungal load.
- The findings provide insights into the pathogenesis and immune response of this opportunistic infection.
