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Minor role played by type I tumour necrosis factor receptor in the control of Mycobacterium avium proliferation in infected mice
Author(s) -
Silva R. A.,
Gomes M. S.,
Appelberg R.
Publication year - 2000
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.2000.00937.x
Subject(s) - biology , virulence , tumor necrosis factor alpha , microbiology and biotechnology , spleen , receptor , mycobacterium , virulence factor , recombinant dna , immunology , necrosis , immune system , cytokine , wild type , bacteria , mutant , gene , genetics
Summary Control of mycobacterial growth depends on the concerted activity of different cytokines acting in different stages of the development of innate and adaptive immune responses. Tumour necrosis factor‐α (TNF‐α) has been shown to play a protective role in Mycobacterium avium infections. Here we assessed the growth of this mycobacterial species in wild‐type mice and in mice with a genetically engineered disruption of the type I receptor for TNF‐α (p55‐KO mice). p55‐KO mice infected with a low‐virulence strain of M. avium exhibited a slightly delayed capacity to eliminate the micro‐organisms from the liver as compared with wild‐type animals. However, either the growth of this strain in the other organs studied (spleen and lung) or the growth of two other strains of M. avium with intermediate or high virulence, failed to be affected by mutation of the TNF‐α receptor. p55‐KO mice were also as protected by the administration of recombinant interleukin‐12 as the heterozygous p55 +/– mice. We conclude that signalling through the type I TNF receptor plays a small role in vivo in the induction of mycobacteriostasis during M. avium infection but may improve survival during infection with virulent mycobacteria, independently of the extent of their proliferation.