PMID- 10679105
OWN - NLM
STAT- MEDLINE
DCOM- 20000323
LR  - 20220414
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 164
IP  - 5
DP  - 2000 Mar 1
TI  - Role of CC chemokines (macrophage inflammatory protein-1 beta, monocyte 
      chemoattractant protein-1, RANTES) in acute lung injury in rats.
PG  - 2650-9
AB  - The role of the CC chemokines, macrophage inflammatory protein-1 beta (MIP-1 
      beta), monocyte chemotactic peptide-1 (MCP-1), and RANTES, in acute lung 
      inflammatory injury induced by intrapulmonary deposition of IgG immune complexes 
      injury in rats was determined. Rat MIP-1 beta, MCP-1, and RANTES were cloned, the 
      proteins were expressed, and neutralizing Abs were developed. mRNA and protein 
      expression for MIP-1 beta and MCP-1 were up-regulated during the inflammatory 
      response, while mRNA and protein expression for RANTES were constitutive and 
      unchanged during the inflammatory response. Treatment of rats with anti-MIP-1 
      beta Ab significantly decreased vascular permeability by 37% (p = 0.012), reduced 
      neutrophil recruitment into lung by 65% (p = 0.047), and suppressed levels of 
      TNF-alpha in bronchoalveolar lavage fluids by 61% (p = 0.008). Treatment of rats 
      with anti-rat MCP-1 or anti-rat RANTES had no effect on the development of lung 
      injury. In animals pretreated intratracheally with blocking Abs to MCP-1, RANTES, 
      or MIP-1 beta, significant reductions in the bronchoalveolar lavage content of 
      these chemokines occurred, suggesting that these Abs had reached their targets. 
      Conversely, exogenously MIP-1 beta, but not RANTES or MCP-1, caused enhancement 
      of the lung vascular leak. These data indicate that MIP-1 beta, but not MCP-1 or 
      RANTES, plays an important role in intrapulmonary recruitment of neutrophils and 
      development of lung injury in the model employed. The findings suggest that in 
      chemokine-dependent inflammatory responses in lung CC chemokines do not 
      necessarily demonstrate redundant function.
FAU - Bless, N M
AU  - Bless NM
AD  - Department of Trauma Surgery, University of Freiburg, Freiburg, Germany.
FAU - Huber-Lang, M
AU  - Huber-Lang M
FAU - Guo, R F
AU  - Guo RF
FAU - Warner, R L
AU  - Warner RL
FAU - Schmal, H
AU  - Schmal H
FAU - Czermak, B J
AU  - Czermak BJ
FAU - Shanley, T P
AU  - Shanley TP
FAU - Crouch, L D
AU  - Crouch LD
FAU - Lentsch, A B
AU  - Lentsch AB
FAU - Sarma, V
AU  - Sarma V
FAU - Mulligan, M S
AU  - Mulligan MS
FAU - Friedl, H P
AU  - Friedl HP
FAU - Ward, P A
AU  - Ward PA
LA  - eng
GR  - HL31963/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Antibodies, Blocking)
RN  - 0 (Antigen-Antibody Complex)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL4)
RN  - 0 (Chemokine CCL5)
RN  - 0 (Chemokines, CC)
RN  - 0 (Immune Sera)
RN  - 0 (Immunoglobulin G)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Recombinant Proteins)
SB  - IM
MH  - Acute Disease
MH  - Animals
MH  - Antibodies, Blocking/administration & dosage
MH  - Antigen-Antibody Complex/toxicity
MH  - Bronchoalveolar Lavage Fluid/immunology
MH  - Chemokine CCL2/administration & dosage/antagonists & 
      inhibitors/genetics/*physiology
MH  - Chemokine CCL4
MH  - Chemokine CCL5/administration & dosage/antagonists & 
      inhibitors/genetics/*physiology
MH  - Chemokines, CC/administration & dosage/antagonists & 
      inhibitors/genetics/*physiology
MH  - Chemotaxis, Leukocyte/immunology
MH  - Cloning, Molecular
MH  - Immune Sera/administration & dosage
MH  - Immunoglobulin G/toxicity
MH  - Intubation, Intratracheal
MH  - Lung/*immunology/metabolism/*pathology
MH  - Macrophage Inflammatory Proteins/administration & dosage/antagonists & 
      inhibitors/genetics/*physiology
MH  - Male
MH  - Pulmonary Alveoli/immunology/pathology
MH  - RNA, Messenger/biosynthesis
MH  - Rats
MH  - Rats, Long-Evans
MH  - Recombinant Proteins/biosynthesis/immunology
EDAT- 2000/02/29 09:00
MHDA- 2000/03/25 09:00
CRDT- 2000/02/29 09:00
PHST- 2000/02/29 09:00 [pubmed]
PHST- 2000/03/25 09:00 [medline]
PHST- 2000/02/29 09:00 [entrez]
AID - ji_v164n5p2650 [pii]
AID - 10.4049/jimmunol.164.5.2650 [doi]
PST - ppublish
SO  - J Immunol. 2000 Mar 1;164(5):2650-9. doi: 10.4049/jimmunol.164.5.2650.