Open AccessCytokine gene expression in the lungs of BALB/c mice during primary and secondary intranasal infection with Mycoplasma pneumoniae
Author(s) -
Klaus Pietsch,
Stefan Ehlers,
Enno Jacobs
Publication year - 1994
Publication title -
microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.352
H-Index - 35
eISSN - 1465-2080
pISSN - 1350-0872
DOI - 10.1099/13500872-140-8-2043
Subject(s) - mycoplasma pneumoniae , biology , proinflammatory cytokine , spleen , gene expression , immunology , cytokine , pathogenesis , tumor necrosis factor alpha , innate immune system , mycoplasma , immune system , gene , microbiology and biotechnology , inflammation , medicine , biochemistry , pneumonia
Cytokine gene expression was determined in vivo in the lungs and spleens of Mycoplasma pneumoniae-infected BALB/c mice by means of qualitative and semiquantitative PCR-mediated mRNA amplification. During the acute phase of both primary and secondary infections, cytokines commonly associated with innate resistance, TNF alpha, IFN gamma, IL-1 beta and IL-6, were expressed. In contrast, early expression of the genes for IL-2 and IL-2 receptor was detected only during reinfection. Expression was greater in the lungs than in the spleen, attesting to the rapid accumulation of lymphocytes at the infected site. Interestingly, IL-2 mRNA expression declined rapidly and was no longer detectable after 24 h, whereas IL-10 mRNA levels rose sharply during the same period. During reinfection, mRNAs for TNF alpha and IL-6 were 10-fold and for IFN gamma about 50-fold higher than during primary challenge. The results suggest that the pathogenesis of M. pneumoniae diseases may be associated with elevated expression of proinflammatory cytokines.