PMID- 10204577
OWN - NLM
STAT- MEDLINE
DCOM- 19990429
LR  - 20190516
IS  - 0741-5400 (Print)
IS  - 0741-5400 (Linking)
VI  - 65
IP  - 4
DP  - 1999 Apr
TI  - Functional roles of MCP-1 in Propionibacterium acnes-induced, T cell-mediated 
      pulmonary granulomatosis in rabbits.
PG  - 482-91
AB  - The immunological manifestation of granuloma formations in humans largely depends 
      on the delayed-type hypersensitivity response. We investigated the involvement of 
      monocyte chemoattractant protein-1 (MCP-1) in a rabbit model of T cell-mediated 
      pulmonary granulomatosis. Intravenous injection of Propionibacterium acnes (P. 
      acnes) into sensitized rabbits induced massive and diffuse pulmonary granulomas. 
      Levels of MCP-1 in sera and bronchoalveolar lavage fluids (BALF) peaked before 
      the granuloma formation reached the peak (on days 1 and 3 after challenge, 
      respectively). Chemotactic activities toward monocytes and T cells in BALF were 
      inhibited by anti-MCP-1 IgG by 80 and 36%, respectively. The phenotypic analysis 
      of the migrating T cells revealed that activated and memory T cells rather than 
      naive cells were preferentially attracted to the BALF. Administration of 
      anti-MCP-1 antiserum inhibited the development of granuloma formation in both 
      size and number, the numbers of infiltrating leukocytes in BALF, the expression 
      of adhesion molecules on peripheral monocytes/T cells, and on macrophages/T cells 
      in BALF, and the production of TNF-alpha in the lung. Anti-MCP-1 resulted in a 
      trend toward decreased level of IL-1beta in the lung. The inhibition of the 
      production of these cytokines appeared to be induced indirectly through the 
      inhibition of the recruitment of macrophages that produce these cytokines. The 
      results suggest important roles of MCP-1 in the development of granuloma 
      formation in this model through the attraction and activation of specific types 
      of cells.
FAU - Ichiyasu, H
AU  - Ichiyasu H
AD  - First Department of Internal Medicine, Kumamoto University School of Medicine, 
      Japan.
FAU - Suga, M
AU  - Suga M
FAU - Matsukawa, A
AU  - Matsukawa A
FAU - Iyonaga, K
AU  - Iyonaga K
FAU - Mizobe, T
AU  - Mizobe T
FAU - Takahashi, T
AU  - Takahashi T
FAU - Ando, M
AU  - Ando M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Leukoc Biol
JT  - Journal of leukocyte biology
JID - 8405628
RN  - 0 (Chemokine CCL2)
RN  - 0 (Immune Sera)
RN  - 0 (Interleukin-1)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Bronchoalveolar Lavage Fluid/chemistry/cytology
MH  - Chemokine CCL2/metabolism/*physiology
MH  - Female
MH  - Gram-Positive Bacterial Infections/*immunology/pathology
MH  - Granuloma, Respiratory Tract/etiology/*immunology/pathology
MH  - Immune Sera/pharmacology
MH  - Interleukin-1/biosynthesis
MH  - Pneumonia, Bacterial/*immunology/pathology
MH  - Propionibacterium acnes/*immunology
MH  - Rabbits
MH  - T-Lymphocytes/*immunology
MH  - Tumor Necrosis Factor-alpha/biosynthesis
EDAT- 1999/04/16 00:00
MHDA- 1999/04/16 00:01
CRDT- 1999/04/16 00:00
PHST- 1999/04/16 00:00 [pubmed]
PHST- 1999/04/16 00:01 [medline]
PHST- 1999/04/16 00:00 [entrez]
AID - 10.1002/jlb.65.4.482 [doi]
PST - ppublish
SO  - J Leukoc Biol. 1999 Apr;65(4):482-91. doi: 10.1002/jlb.65.4.482.