Pneumocystis carinii infection in young non-immunosuppressed rabbits. Kinetics of infection and of the primary specific immune response

Citation
E. Tamburrini et al., Pneumocystis carinii infection in young non-immunosuppressed rabbits. Kinetics of infection and of the primary specific immune response, MED MICROBI, 188(1), 1999, pp. 1-7
Citations number
38
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Microbiology
Journal title
MEDICAL MICROBIOLOGY AND IMMUNOLOGY
ISSN journal
0300-8584 → ACNP
Volume
188
Issue
1
Year of publication
1999
Pages
1 - 7
Database
ISI
SICI code
0300-8584(199908)188:1<1:PCIIYN>2.0.ZU;2-R
Abstract
The aim of this study was to determine the kinetics, the dissemination of t he infection and the immunological response to Pneumocystis carinii primary infection in a non-immunosuppressed rabbit model. For this purpose, we dev eloped a nested PCR that amplified a portion of the mitochondrial large-sub unit rRNA gene of rabbit-derived P. carinii. The PCR detected P. carinii DN A in lung and bronchoalveolar lavage fluids from 14- to 45-day-old rabbits but not in their serum. No P. carinii DNA was detected in extrapulmonary or gans from 28-day-old rabbits with P. carinii pneumonia. ELISA and immunoblo tting analysis showed that 5-day-old pups had elevated specific IgG. The Ig G concentration sharply decreased, reaching a trough on day 21, and from th en onwards progressively increased as the infection cleared. Conversely, th e specific IgM concentration increased during the infection and peaked on d ay 28. IgG mainly recognized a 50-kDa subunit of P. carinii organisms; IgM recognized first a 45-kDa subunit on day 21, whereas from day 28 onwards it also recognized the 50-kDa subunit. A P. carinii-specific splenocyte proli ferative response was observed on day 45. These findings suggest that P. ca rinii primary infection is a time-limited and a lung-limited event and cont ribute new information on the relationship between the kinetics of primary P. carinii infection and the immunological response in a model that mimics the primary infections in humans.