PMID- 10882225
OWN - NLM
STAT- MEDLINE
DCOM- 20000714
LR  - 20071115
IS  - 0022-2143 (Print)
IS  - 0022-2143 (Linking)
VI  - 136
IP  - 1
DP  - 2000 Jul
TI  - Mediators of hypersensitivity pneumonitis.
PG  - 29-38
AB  - Inhalation of Saccharopolyspora rectivirgula (S. rectivirgula) causes farmer's 
      lung disease, a classic example of hypersensitivity pneumonitis (HP). HP is 
      characterized by bronchoalveolar lavage fluid (BALF) neutrophilia (within the 
      first 48 hours after inhalation), followed by BALF lymphocytosis. We utilized a 
      well-described murine model of HP to determine the timing of the appearance of 
      the C-C chemokines monocyte chemoattractant protein-1 (MCP-1) and macrophage 
      inflammatory protein-1alpha (MIP-1alpha); the inflammatory cytokines tumor 
      necrosis factor (TNF), interleukin-1alpha (IL-1alpha), and interleukin-6 (IL-6); 
      and the Th1 -differentiating cytokine interleukin-12 (IL-12) in BALF. After a 
      single intratracheal administration of S. rectivirgula, there was remarkable BALF 
      neutrophilia (peak 24 to 48 hours), followed by a BALF lymphocytosis (peak 48 to 
      72 hours) in both C57Bl/6 and BALB/c mice that was preceded by the appearance of 
      MIP-1alpha in BALF (peak 4 to 6 hours) and MCP-1 (peak at 48 hours). In both 
      strains of mice there was a striking increase of BALF IL-12 (peak 48 to 72 
      hours). There was also an increase in BALF IL-6, IL-1alpha, and TNF that was 
      greater in the BALB/c mice than in the C57Bl/6 mice. S. rectivirgula induced the 
      secretion of MIP-1alpha, MCP-1, IL-6, IL-1alpha, and IL-12 from the murine 
      macrophage cell line J774A.1; MIP-1alpha, IL-6, IL-1alpha, IL-12, and TNF from 
      C57Bl/6 alveolar macrophages; and IL-1alpha, IL-6, and TNF-but not IL-12-from 
      BALB/c alveolar macrophages. We conclude that chemokines and cytokines induced by 
      intratracheal administration of S. rectivirgula precede BALF neutrophilia and 
      lymphocytosis and may cause differentiation of Th1 cells; we also conclude that 
      pulmonary macrophages represent a potential source of these substances.
FAU - Schuyler, M
AU  - Schuyler M
AD  - Department of Medicine, Albuquerque Veterans Affairs Medical Center, University 
      of New Mexico School of Medicine, 87108, USA.
FAU - Gott, K
AU  - Gott K
FAU - Cherne, A
AU  - Cherne A
LA  - eng
GR  - HL44253/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Lab Clin Med
JT  - The Journal of laboratory and clinical medicine
JID - 0375375
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL3)
RN  - 0 (Chemokine CCL4)
RN  - 0 (Interleukin-6)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 187348-17-0 (Interleukin-12)
SB  - IM
CIN - J Lab Clin Med. 2000 Jul;136(1):5-6. PMID: 10882221
MH  - Alveolitis, Extrinsic Allergic/*immunology/*pathology
MH  - Animals
MH  - Bronchoalveolar Lavage Fluid/cytology
MH  - Chemokine CCL2/metabolism
MH  - Chemokine CCL3
MH  - Chemokine CCL4
MH  - Interleukin-12/metabolism
MH  - Interleukin-6/metabolism
MH  - Leukocyte Count
MH  - Lymphocytes
MH  - Macrophage Inflammatory Proteins/metabolism
MH  - Macrophages
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Neutrophils
MH  - Tumor Necrosis Factor-alpha/metabolism
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 - S0022-2143(00)89787-5 [pii]
AID - 10.1067/mlc.2000.107694 [doi]
PST - ppublish
SO  - J Lab Clin Med. 2000 Jul;136(1):29-38. doi: 10.1067/mlc.2000.107694.