PMID- 10849364
OWN - NLM
STAT- MEDLINE
DCOM- 20000706
LR  - 20190818
IS  - 0300-9475 (Print)
IS  - 0300-9475 (Linking)
VI  - 51
IP  - 6
DP  - 2000 Jun
TI  - In situ expression of cytokines and cellular phenotypes in the lungs of mice with 
      slowly progressive primary tuberculosis.
PG  - 548-56
AB  - The cellular phenotypes and the expression of cytokines were studied in the lungs 
      of mice, using immunohistochemistry, during different phases of slowly 
      progressive primary murine tuberculosis infection. During the first phase the 
      small focal lesions in healthy mice contained predominantly interleukin-2 
      (IL-2)-expressing cells. A small number of tumour necrosis factor-alpha 
      (TNF-alpha)-, monocyte chemoattractant protein-1 (MCP-1)- and IL-10-expressing 
      cells were also present. IL-4-expressing cells were not detected. During the 
      second phase the mice became unwell, but the bacterial counts and the size of 
      focal lesions stabilized. IL-4-expressing cells appeared. The IL-10-, TNF-alpha- 
      and MCP-1-expressing cells increased in number. On progression to phase three, 
      the mice became seriously unwell and died rapidly. The inflammation spread to 
      approximately 80% of the lung parenchyma. There was a marked increase in the 
      number of IL-10-expressing cells. Expression of other cytokines was similar to 
      that observed in the second phase. In the lesions, 3-6% of the macrophages (Mphi) 
      containing mycobacterial antigens expressed high levels of IL-10 and TNF-alpha. 
      The absolute numbers of CD3-, CD4- and CD11b-expressing cells in the lesions 
      increased with the progression of infection. The numbers of CD8+ cells were 
      reduced in the last phase of infection. The kinetics of T-lymphocyte subsets and 
      the pattern of cytokine expression changed with the type and degree of tissue 
      injury. The small number of Mphi with a heavy load of mycobacterial antigens may 
      be the cause of this disturbance in cytokine balance, thus leading to progression 
      of inflammation.
FAU - Mustafa, T
AU  - Mustafa T
AD  - Department of Odontology, University of Bergen, Norway.
FAU - Phyu, S
AU  - Phyu S
FAU - Nilsen, R
AU  - Nilsen R
FAU - Jonsson, R
AU  - Jonsson R
FAU - Bjune, G
AU  - Bjune G
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Scand J Immunol
JT  - Scandinavian journal of immunology
JID - 0323767
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-2)
RN  - 0 (Macrophage-1 Antigen)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 130068-27-8 (Interleukin-10)
RN  - 207137-56-2 (Interleukin-4)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2/biosynthesis/immunology
MH  - Cytokines/*biosynthesis
MH  - Female
MH  - Immunophenotyping
MH  - Interleukin-10/biosynthesis/immunology
MH  - Interleukin-2/biosynthesis/immunology
MH  - Interleukin-4/biosynthesis/immunology
MH  - Kinetics
MH  - Leukocytes, Mononuclear/immunology/metabolism
MH  - Lung/*immunology/*metabolism
MH  - Macrophage-1 Antigen/analysis/biosynthesis
MH  - Macrophages/immunology/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mycobacterium tuberculosis/growth & development/*immunology
MH  - Tuberculosis/*immunology/metabolism/pathology
MH  - Tumor Necrosis Factor-alpha/biosynthesis/immunology
EDAT- 2000/06/10 09:00
MHDA- 2000/07/08 11:00
CRDT- 2000/06/10 09:00
PHST- 2000/06/10 09:00 [pubmed]
PHST- 2000/07/08 11:00 [medline]
PHST- 2000/06/10 09:00 [entrez]
AID - sji721 [pii]
AID - 10.1046/j.1365-3083.2000.00721.x [doi]
PST - ppublish
SO  - Scand J Immunol. 2000 Jun;51(6):548-56. doi: 10.1046/j.1365-3083.2000.00721.x.