<i>Pneumocystis carinii</i>
            f. sp.
            <i>hominis</i>
            Is Not Infectious for SCID mice

Durand-Joly, Isabelle; Aliouat, El Moukhtar; Recourt, C.; Guyot, Karine; François, Nadine; Wauquier, Michèle; Camus, Daniel; Dei‐Cas, Eduardo

doi:10.1128/jcm.40.5.1862-1865.2002

Cited by 77 publications

(29 citation statements)

References 21 publications

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“…Eight weeks postinfection, all animals harbored a high P. carinii burden and were euthanized. Their lungs were dissected to isolate organisms that were cryopreserved while remaining highly infectious [12,24,25]. …”

Section: Methodsmentioning

confidence: 99%

Growth and Airborne Transmission of Cell-Sorted Life Cycle Stages of Pneumocystis carinii

et al. 2013

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Pneumocystis organisms are airborne opportunistic pathogens that cannot be continuously grown in culture. Consequently, the follow-up of Pneumocystis stage-to-stage differentiation, the sequence of their multiplication processes as well as formal identification of the transmitted form have remained elusive. The successful high-speed cell sorting of trophic and cystic forms is paving the way for the elucidation of the complex Pneumocystis life cycle. The growth of each sorted Pneumocystis stage population was followed up independently both in nude rats and in vitro. In addition, by setting up a novel nude rat model, we attempted to delineate which cystic and/or trophic forms can be naturally aerially transmitted from host to host. The results showed that in axenic culture, cystic forms can differentiate into trophic forms, whereas trophic forms are unable to evolve into cystic forms. In contrast, nude rats inoculated with pure trophic forms are able to produce cystic forms and vice versa. Transmission experiments indicated that 12 h of contact between seeder and recipient nude rats was sufficient for cystic forms to be aerially transmitted. In conclusion, trophic- to cystic-form transition is a key step in the proliferation of Pneumocystis microfungi because the cystic forms (but not the trophic forms) can be transmitted by aerial route from host to host.

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Section: Methodsmentioning

confidence: 99%

Growth and Airborne Transmission of Cell-Sorted Life Cycle Stages of Pneumocystis carinii

et al. 2013

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“…This study demonstrated that Pneumocystis could not be transmitted between mice and ferrets [6]. This observation was soon followed by similar results that showed Pneumocystis from rabbits, rats, monkeys, and humans were not infectious for mice [reviewed in 7]. Thus, available data indicates that each mammalian species that contracts PcP has its own strain or species of Pneumocystis .…”

Section: Pneumocystis Is Not a Zoonosismentioning

confidence: 96%

Pneumocystis: Where Does It Live?

Gigliotti

Wright²

2012

PLoS Pathog

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“…Pneumocystis organisms recovered from different mammalian hosts are genetically distinct, and attempts at cross-species transmission have not been successful [1–3]. Furthermore, the requirements for Pneumocystis growth in vitro have not been determined, making the study of life cycle and biology a significant challenge.…”

Section: Introductionmentioning

confidence: 99%

Selective Ablation of Lung Epithelial IKK2 Impairs Pulmonary Th17 Responses and Delays the Clearance of Pneumocystis

Pérez-Nazario

Rangel-Moreno

O’Reilly

et al. 2013

The Journal of Immunology

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Pneumocystis is an atypical fungal pathogen which causes severe, often fatal pneumonia (PcP) in immunocompromised patients. Healthy humans and animals also encounter this pathogen, but generate a protective CD4+ T cell dependent immune response that clears the pathogen with little evidence of disease. Pneumocystis organisms attach tightly to respiratory epithelial cells, and in vitro studies have demonstrated that this interaction triggers NF-κB-dependent epithelial cell responses. However, the contribution of respiratory epithelial cells to the normal host response to Pneumocystis remains unknown. Inhibitor of κB Kinase 2 (IKK2) is the upstream kinase that is critical for inducible NF-κB activation. To determine whether IKK2-dependent lung epithelial cell responses contribute to the anti-Pneumocystis immune response in vivo, transgenic mice with lung epithelial cell-specific deletion of IKK2 (IKK2ΔLEC) were generated. Compared to wild type mice, IKK2ΔLEC mice exhibited a delayed onset of Th17 and B cell responses in the lung, and delayed fungal clearance. Importantly, delayed Pneumocystis clearance in IKK2ΔLEC mice was associated with an exacerbated immune response, impaired pulmonary function, and altered lung histology. These data demonstrate that IKK2-dependent lung epithelial cell responses are important regulators of pulmonary adaptive immune responses, and are required for optimal host defense against Pneumocystis infection. LECs likely set the threshold for initiation of the pulmonary immune response, and serve to prevent exacerbated lung inflammation by promoting the rapid control of respiratory fungal infection.

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Pneumocystis carinii f. sp. hominis Is Not Infectious for SCID mice

Cited by 77 publications

References 21 publications

Growth and Airborne Transmission of Cell-Sorted Life Cycle Stages of Pneumocystis carinii

Growth and Airborne Transmission of Cell-Sorted Life Cycle Stages of Pneumocystis carinii

Pneumocystis: Where Does It Live?

Selective Ablation of Lung Epithelial IKK2 Impairs Pulmonary Th17 Responses and Delays the Clearance of Pneumocystis

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