PMID- 8711735
OWN - NLM
STAT- MEDLINE
DCOM- 19960911
LR  - 20211203
IS  - 0300-483X (Print)
IS  - 0300-483X (Linking)
VI  - 111
IP  - 1-3
DP  - 1996 Jul 17
TI  - Characterization of histamine releasing factors in diisocyanate-induced 
      occupational asthma.
PG  - 191-206
AB  - Immunologic mechanisms contributing to diisocyanate-induced occupational asthma 
      (OA) are poorly defined. There is a relatively low incidence of 
      diisocyanate-specific IgE antibody responses. The frequent occurrence of delayed 
      onset asthmatic responses in workers with diisocyanate asthma suggests a role for 
      cellular immune mechanisms. We have shown in vitro production of antigen-specific 
      mononuclear cell-derived histamine releasing factors (HRF) by peripheral blood 
      mononuclear cells (PBMCs) of workers with OA. Monocyte chemoattractant protein-1 
      (MCP-1) and RANTES (acronym for "regulated on activation normal T expressed and 
      secreted") are chemokines found in PBMC supernatants that express HRF activity. 
      Diisocyanate-exposed workers were tested for diisocyanate antigen-stimulated 
      enhancement of HRF, MCP-1, and RANTES production in supernatants of PBMCs and for 
      serum specific IgE and IgG antibody levels to diisocyanate antigens bound to 
      human serum albumin (HSA). PBMCs of workers with diisocyanate OA showed 
      significantly increased production of antigen-specific HRF activity and MCP-1 ( > 
      300 ng/ml) compared to diisocyanate-exposed asymptomatic workers (P < 0.05). 
      Antigen-stimulated enhancement of MCP-1 mRNA was demonstrated by 
      reverse-transcription PCR. RANTES mRNA and chemokine secretion ( < 1 ng/ml) was 
      also demonstrated in PBMCs, but did not show antigen enhancement in OA workers. 
      Hapten specificity for the diisocyanate chemical to which a patient had been 
      exposed was demonstrated for HRF enhancement and for IgG antibody reactions, but 
      not for IgE reactions. HRF production was demonstrated in PBMC subpopulations, 
      including lymphocytes and purified T cells. OA subjects showed increased CD8+ 
      cells by immunofluorescence (mean CD4+: CD8+ = 1.2 +/- 0.2). The results suggest 
      that diisocyanate antigen enhancement of HRF and MCP-1 production are stimulated 
      by hapten-specific T cell reactions. Since a weak association has been found 
      between IgE antibody synthesis and induction of diisocyanate OA, the role of T 
      cell cytokines and chemokines in the pathogenesis of OA requires further 
      investigation.
FAU - Lummus, Z L
AU  - Lummus ZL
AD  - Department of Internal Medicine, University of Cincinnati College of Medicine, OH 
      45267-0563, USA.
FAU - Alam, R
AU  - Alam R
FAU - Bernstein, J A
AU  - Bernstein JA
FAU - Bernstein, D I
AU  - Bernstein DI
LA  - eng
GR  - ES06096-02A/ES/NIEHS NIH HHS/United States
GR  - K01 0H00073/PHS HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Ireland
TA  - Toxicology
JT  - Toxicology
JID - 0361055
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (Epitopes)
RN  - 0 (Isocyanates)
RN  - 0 (Lymphokines)
RN  - 0 (Tumor Protein, Translationally-Controlled 1)
SB  - IM
MH  - Asthma/*chemically induced/immunology/metabolism
MH  - Base Sequence
MH  - *Biomarkers, Tumor
MH  - Epitopes/analysis
MH  - Female
MH  - Histamine Release/*drug effects
MH  - Humans
MH  - Isocyanates/*adverse effects/immunology
MH  - Leukocytes, Mononuclear/classification/immunology/metabolism
MH  - Lymphokines/biosynthesis/*chemistry/immunology
MH  - Male
MH  - Molecular Sequence Data
MH  - Occupational Diseases/*chemically induced/metabolism
MH  - Tumor Protein, Translationally-Controlled 1
EDAT- 1996/07/17 00:00
MHDA- 1996/07/17 00:01
CRDT- 1996/07/17 00:00
PHST- 1996/07/17 00:00 [pubmed]
PHST- 1996/07/17 00:01 [medline]
PHST- 1996/07/17 00:00 [entrez]
AID - 0300-483X(96)03376-8 [pii]
AID - 10.1016/0300-483x(96)03376-8 [doi]
PST - ppublish
SO  - Toxicology. 1996 Jul 17;111(1-3):191-206. doi: 10.1016/0300-483x(96)03376-8.