PMID- 7527830
OWN - NLM
STAT- MEDLINE
DCOM- 19950119
LR  - 20190516
IS  - 0741-5400 (Print)
IS  - 0741-5400 (Linking)
VI  - 56
IP  - 6
DP  - 1994 Dec
TI  - Kinetics of macrophage subpopulations and expression of monocyte chemoattractant 
      protein-1 (MCP-1) in bleomycin-induced lung injury of rats studied by a novel 
      monoclonal antibody against rat MCP-1.
PG  - 741-50
AB  - We investigated the kinetics of macrophage subpopulations and the expression of 
      monocyte chemoattractant protein 1 (MCP-1) in a rat model of bleomycin-induced 
      lung injury. Rat macrophage subpopulations were examined by immunohistochemistry 
      using various anti-rat macrophage monoclonal antibodies (mAbs) and their 
      proliferative capacity by [3H]thymidine (3HTdR) autoradiography. To detect the 
      localization of expressed MCP-1, we generated an mAb against rat MCP-1 for 
      immunohistochemical staining. Expression of MCP-1 messenger RNA (mRNA) was 
      detected by Northern blot hybridization. Shortly after intratracheal instillation 
      of bleomycin, the number of exudate macrophages recognized by mAb TRPM-3 
      increased in the injured lungs, peaked 3 days later, and decreased thereafter, 
      whereas tissue macrophages identified by mAb ED2 increased slowly and peaked 2 
      weeks after instillation. Northern blot analysis disclosed that the expression of 
      MCP-1 mRNA in the lung was most prominent 1 day after instillation and declined 
      thereafter, preceding the numerical change of the TRPM-3-positive exudate 
      macrophages. Immunohistochemistry with anti-rat MCP-1 revealed that the main 
      sources of MCP-1 production were alveolar and interstitial macrophages and 
      polymorphonuclear leukocytes. Based on these results, MCP-1 produced by 
      polymorphonuclear leukocytes and by alveolar and interstitial macrophages is 
      thought to induce the infiltration of blood monocytes, and infiltrated exudate 
      macrophages produce MCP-1 to enhance subsequent accumulation of macrophages. In 
      contrast, the expression of MCP-1 did not correlate with the numerical changes of 
      the ED2-positive macrophages.
FAU - Sakanashi, Y
AU  - Sakanashi Y
AD  - Second Department of Pathology, Kumamoto University School of Medicine, Japan.
FAU - Takeya, M
AU  - Takeya M
FAU - Yoshimura, T
AU  - Yoshimura T
FAU - Feng, L
AU  - Feng L
FAU - Morioka, T
AU  - Morioka T
FAU - Takahashi, K
AU  - Takahashi K
LA  - eng
PT  - Journal Article
PL  - England
TA  - J Leukoc Biol
JT  - Journal of leukocyte biology
JID - 8405628
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemotactic Factors)
RN  - 0 (RNA, Messenger)
RN  - 10028-17-8 (Tritium)
RN  - 11056-06-7 (Bleomycin)
RN  - VC2W18DGKR (Thymidine)
SB  - IM
MH  - Animals
MH  - Antibodies, Monoclonal/biosynthesis
MH  - Autoradiography
MH  - Base Sequence
MH  - Bleomycin/*toxicity
MH  - Blotting, Northern
MH  - Cell Cycle
MH  - Cell Division
MH  - Chemokine CCL2
MH  - Chemotactic Factors/analysis/immunology/*physiology
MH  - Disease Models, Animal
MH  - Fibrosis
MH  - Immunohistochemistry
MH  - Lung/chemistry/cytology/drug effects
MH  - Lung Diseases/chemically induced/*metabolism/*pathology
MH  - Macrophages/*cytology/*metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Molecular Sequence Data
MH  - RNA, Messenger/analysis
MH  - Rats
MH  - Rats, Wistar
MH  - Thymidine/metabolism
MH  - Tritium
EDAT- 1994/12/01 00:00
MHDA- 1994/12/01 00:01
CRDT- 1994/12/01 00:00
PHST- 1994/12/01 00:00 [pubmed]
PHST- 1994/12/01 00:01 [medline]
PHST- 1994/12/01 00:00 [entrez]
AID - 10.1002/jlb.56.6.741 [doi]
PST - ppublish
SO  - J Leukoc Biol. 1994 Dec;56(6):741-50. doi: 10.1002/jlb.56.6.741.