PMID- 9723671
OWN - NLM
STAT- MEDLINE
DCOM- 19980925
LR  - 20211203
IS  - 0091-6749 (Print)
IS  - 0091-6749 (Linking)
VI  - 102
IP  - 2
DP  - 1998 Aug
TI  - Diisocyanate antigen-enhanced production of monocyte chemoattractant protein-1, 
      IL-8, and tumor necrosis factor-alpha by peripheral mononuclear cells of workers 
      with occupational asthma.
PG  - 265-74
AB  - BACKGROUND: Previous studies have shown a significant association between 
      confirmed diisocyanate-induced asthma (DOA) and in vitro production of 
      diisocyanate antigen-stimulated histamine-releasing factors by PBMCs. Chemokines 
      found in PBMC supernatants are known to express histamine-releasing factor 
      activity. OBJECTIVE: PBMCs of diisocyanate-exposed workers were tested in vitro 
      for diisocyanate antigen-specific enhancement of monocyte chemoattractant 
      protein-1 (MCP-1), monocyte chemoattractant protein-3 (MCP-3), macrophage 
      inflammatory protein-1alpha, RANTES, IL-8, and T-cell cytokines that could play a 
      regulatory role in chemokine synthesis (IL-4, IL-5, IFN-gamma, and TNF-alpha. 
      METHODS: Secretion of chemokines and cytokines was determined by quantitative 
      immunochemical assays of PBMC supernatants. Synthesis of mRNA for beta-chemokines 
      was determined by reverse transcription-polymerase chain reaction. RESULTS: PBMCs 
      of workers with DOA showed significantly enhanced secretion for MCP-1 compared 
      with diisocyanate-exposed asymptomatic workers (P < .05). In vitro induction of 
      antigen-stimulated MCP-1 mRNA synthesis in cultured PBMCs was demonstrated by 
      reverse-transcription polymerase chain reaction. Quantitation of cytokines in 
      supernatants showed increased mean production of IL-8 and TNF-alpha. IFN-gamma, 
      IL-4, and IL-5 were not enhanced in subjects with DOA. CONCLUSION: Antigen 
      stimulation of MCP-1 and TNF-alpha suggest that diisocyanate-specific cellular 
      immune reactions result in activation of macrophages, which may be important in 
      the pathogenesis of DOA.
FAU - Lummus, Z L
AU  - Lummus ZL
AD  - Department of Internal Medicine, University of Cincinnati College of Medicine, 
      Ohio 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
PT  - Journal Article
PL  - United States
TA  - J Allergy Clin Immunol
JT  - The Journal of allergy and clinical immunology
JID - 1275002
RN  - 0 (Antigens)
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokines)
RN  - 0 (Cyanates)
RN  - 0 (Interleukin-8)
RN  - 0 (Isocyanates)
RN  - 0 (Lymphokines)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (Tumor Protein, Translationally-Controlled 1)
RN  - 0I70A3I1UF (1,6-hexamethylene diisocyanate)
RN  - 17X7AFZ1GH (Toluene 2,4-Diisocyanate)
RN  - B0LO6BBS8C (4,4'-diphenylmethane diisocyanate)
SB  - IM
MH  - Adult
MH  - Antigens/*immunology
MH  - Asthma/blood/chemically induced/*immunology
MH  - *Biomarkers, Tumor
MH  - Chemokine CCL2/*biosynthesis/genetics
MH  - Chemokines/biosynthesis/genetics
MH  - Cyanates/immunology
MH  - Female
MH  - Humans
MH  - Interleukin-8/*biosynthesis/genetics
MH  - Isocyanates/*immunology
MH  - Leukocytes, Mononuclear/immunology
MH  - Lymphokines/biosynthesis
MH  - Male
MH  - Middle Aged
MH  - Occupational Diseases/blood/chemically induced/*immunology
MH  - Toluene 2,4-Diisocyanate/immunology
MH  - Tumor Necrosis Factor-alpha/*biosynthesis/genetics
MH  - Tumor Protein, Translationally-Controlled 1
EDAT- 1998/09/02 00:00
MHDA- 1998/09/02 00:01
CRDT- 1998/09/02 00:00
PHST- 1998/09/02 00:00 [pubmed]
PHST- 1998/09/02 00:01 [medline]
PHST- 1998/09/02 00:00 [entrez]
AID - S0091674998002723 [pii]
AID - 10.1016/s0091-6749(98)70095-8 [doi]
PST - ppublish
SO  - J Allergy Clin Immunol. 1998 Aug;102(2):265-74. doi: 
      10.1016/s0091-6749(98)70095-8.