PMID- 10879741
OWN - NLM
STAT- MEDLINE
DCOM- 20000717
LR  - 20230216
IS  - 0023-6837 (Print)
IS  - 0023-6837 (Linking)
VI  - 80
IP  - 6
DP  - 2000 Jun
TI  - Correction of defective host response to Mycobacterium bovis BCG infection in 
      TNF-deficient mice by bone marrow transplantation.
PG  - 901-14
AB  - Tumour necrosis factor-alpha (TNF) plays a central role in the recruitment and 
      activation of mononuclear cells in mycobacterial infection. In the absence of 
      type 1 TNF receptor, Mycobacterium bovis Bacillus Calmette-Guerin (BCG) infection 
      of mice is not contained, leading to fatal disease. Because type 1 TNF receptor 
      binds both TNF and lymphotoxin-a, we used TNF-deficient mice to determine the 
      specific role of TNF in the host resistance to BCG infection. The bacterial 
      burden of the lungs of TNF-deficient mice was substantially increased and the 
      mice succumbed to pneumonia between 8 and 12 weeks with a defective granuloma 
      response. Atypical granulomas developed by 4 weeks expressing low levels of MHC 
      class II, intracellular adhesion molecule (ICAM-1), CD11b and CD11c. Macrophages 
      showed little signs of activation and had low levels of acid phosphatase activity 
      and inducible nitric oxide synthase (INOS) expression. Despite the defective 
      cellular recruitment, the chemokines, monocyte chemoattractant protein-1 (MCP-1) 
      and macrophage inflammatory protein-1 (MIP-1alpha), were increased in 
      broncho-alveolar lavage fluid of TNF-deficient mice. The defective host response 
      was corrected by the transplantation of normal bone marrow cells into irradiated 
      TNF-deficient mice. These results demonstrate that TNF derived from hemopoietic 
      cells rather than from mesenchymal origin are essential for a normal host 
      response to BCG infection. Furthermore, TNF dependent expression of adhesion 
      molecules may be essential for the recruitment of mononuclear cells for the 
      formation of bactericidal BCG granulomas.
FAU - Jacobs, M
AU  - Jacobs M
AD  - Department of Immunology, University of Cape Town, South Africa.
FAU - Marino, M W
AU  - Marino MW
FAU - Brown, N
AU  - Brown N
FAU - Abel, B
AU  - Abel B
FAU - Bekker, L G
AU  - Bekker LG
FAU - Quesniaux, V J
AU  - Quesniaux VJ
FAU - Fick, L
AU  - Fick L
FAU - Ryffel, B
AU  - Ryffel B
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Lab Invest
JT  - Laboratory investigation; a journal of technical methods and pathology
JID - 0376617
RN  - 0 (Antigens, CD)
RN  - 0 (Histocompatibility Antigens Class II)
RN  - 0 (Integrin alphaXbeta2)
RN  - 0 (Macrophage-1 Antigen)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - EC 3.1.3.2 (Acid Phosphatase)
SB  - IM
MH  - Acid Phosphatase/analysis
MH  - Animals
MH  - Antigens, CD/genetics/*physiology
MH  - *Bone Marrow Transplantation
MH  - Granuloma/microbiology
MH  - Histocompatibility Antigens Class II/analysis
MH  - Immunity, Innate
MH  - Integrin alphaXbeta2/analysis
MH  - Intercellular Adhesion Molecule-1/analysis
MH  - Lung/immunology/microbiology/pathology
MH  - Macrophage-1 Antigen/analysis
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Mycobacterium bovis/*immunology/isolation & purification
MH  - Pneumonia/microbiology
MH  - Receptors, Tumor Necrosis Factor/genetics/*physiology
MH  - Receptors, Tumor Necrosis Factor, Type I
MH  - Tuberculosis/complications/genetics/*immunology
MH  - Tumor Necrosis Factor-alpha/*deficiency/genetics/*immunology
EDAT- 2000/07/06 11:00
MHDA- 2000/07/25 11:00
CRDT- 2000/07/06 11:00
PHST- 2000/07/06 11:00 [pubmed]
PHST- 2000/07/25 11:00 [medline]
PHST- 2000/07/06 11:00 [entrez]
AID - S0023-6837(22)02153-5 [pii]
AID - 10.1038/labinvest.3780094 [doi]
PST - ppublish
SO  - Lab Invest. 2000 Jun;80(6):901-14. doi: 10.1038/labinvest.3780094.