
In vitro and in vivo T cell responses in mice during bronchopulmonary infection with mucoid Pseudomonas aeruginosa
Author(s) -
STEVENSON M. M.,
KONDRATIEVA T. K.,
APT A. S.,
TAM M. F.,
SKAMENE E.
Publication year - 1995
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1995.tb03478.x
Subject(s) - pseudomonas aeruginosa , in vivo , biology , microbiology and biotechnology , immunology , in vitro , antibody , antigen , bacteria , biochemistry , genetics
SUMMARY In vitro and in vivo T cell responses were determined during the course of bronchopulmonary infection with mucoid Pseudomonas aeruginosa. T cell responses were compared in two inbred mouse strains, namely BALB/c mice, which are resistant to the establishment of chronic bronchopulmonary Ps. aeruginosa infection, and C57B1/6 mice, which have high numbers of bacteria in the lungs through 14 days post‐infection. Unseparated lung cells and lung T cells from BALB/c mice exhibited significantly higher in vitro proliferative responses to both heat‐killed Ps. aeruginosa and concanavalin A (Con A) than cells from C57B1/6 mice through 20 days post‐intratracheal infection with 10 4 colony‐forming units (CFU) Ps. aeruginosa. Proliferation of unseparated lung cells but not lung T cells from BALB/c mice infected 6 days previously with 10 5 CFU Ps. aeruginosa was suppressed in response to Con A; these cells were unresponsive to specific antigen. Suppression of lymphocyte proliferation in the lungs of C57B1/6 mice infected with 10 4 CFU Ps. aeruginosa and in BALB/c mice infected with 10 5 CFU was found to be mediated by adherent lung cells via the production of nitric oxide and prostaglandins. Determination of in vivo T cell‐mediated responses in infected mice demonstrated that resistant BALB/c mice had high DTH and low Pseudomonas ‐specific antibody responses, while C57B1/6 mice had low DTH and high antibody levels, in particular, IgG2b and IgM.