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Relationship Between Pneumocystis carinii Burden and the Degree of Host Immunosuppression in an Airborne Transmission Experimental Model
Author(s) -
Khalife Sara,
Chabé Magali,
Gantois Nausicaa,
Audebert Christophe,
Pottier Muriel,
Hlais Sani,
Pinçon Claire,
Chassat Thierry,
Pierrot Christine,
Khalife Jamal,
AliouatDenis CécileMarie,
Aliouat El Moukhtar
Publication year - 2015
Publication title -
journal of eukaryotic microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.067
H-Index - 77
eISSN - 1550-7408
pISSN - 1066-5234
DOI - 10.1111/jeu.12280
Subject(s) - pneumocystis carinii , pneumocystosis , immunosuppression , biology , context (archaeology) , cd8 , transmission (telecommunications) , immunology , opportunistic infection , dexamethasone , immune system , human immunodeficiency virus (hiv) , endocrinology , viral disease , pneumocystis jirovecii , electrical engineering , engineering , paleontology
To quantitatively assess the risk of contamination by Pneumocystis depending on the degree of immunosuppression (ID) of the exposed rat hosts, we developed an animal model, where rats went through different doses of dexamethasone. Then, natural and aerial transmission of Pneumocystis carinii occurred during cohousing of the rats undergoing gradual ID levels (receivers) with nude rats developing pneumocystosis (seeders). Following contact between receiver and seeder rats, the P. carinii burden of receiver rats was determined by toluidine blue ortho staining and by qPCR targeting the dhfr monocopy gene of this fungus. In this rat model, the level of circulating CD4 + and CD8 + T lymphocytes remained significantly stable and different for each dose of dexamethasone tested, thus reaching the goal of a new stable and gradual ID rat model. In addition, an inverse relationship between the P. carinii burden and the level of circulating CD4 + or CD8 + T lymphocytes was evidenced. This rat model may be used to study other opportunistic pathogens or even co‐infections in a context of gradual ID.