PMID- 7611432
OWN - NLM
STAT- MEDLINE
DCOM- 19950815
LR  - 20171213
IS  - 0002-9513 (Print)
IS  - 0002-9513 (Linking)
VI  - 268
IP  - 6 Pt 1
DP  - 1995 Jun
TI  - Modulation of mast cell functions by in vitro ozone exposure.
PG  - L902-10
AB  - Exposure to ozone has been reported to cause increased immediate bronchial 
      reactivity to inhaled allergen in asthmatics. The purpose of these studies was to 
      determine whether ozone induces either spontaneous physiological degranulation or 
      enhanced immunoglobulin E (IgE)-mediated degranulation of mast cells, thus 
      accounting for the in vivo effects noted in asthmatics. A rat mast cell line 
      (RBL-2H3) was exposed to different levels of ozone (0.1, 0.3, 0.5, and 1.0 ppm), 
      covered by different amounts of buffer, and both cytotoxic and nontoxic exposure 
      conditions were determined. In addition to cytotoxicity, spontaneous release of 
      granule products and prostaglandin D2 (PGD2) associated with ozone exposure were 
      assessed. RBL-2H3 cells were also exposed to ozone under noncytotoxic conditions 
      followed by stimulation with alpha-IgE to cross-link membrane-bound IgE and 
      A23187 so that the effect of ozone on stimulated degranulation could be examined. 
      Only exposure conditions associated with cytotoxicity were associated with 
      spontaneous release of mast cell serotonin, indicating no physiologic 
      degranulation due to ozone exposure. Data presented herein also demonstrate that 
      ozone substantially inhibited both IgE- and A23187-induced degranulation. Neither 
      catalase nor superoxide dismutase protected cells from the inhibitory effect of 
      ozone, indicating that ozone does not act through generation of H2O2 or 
      superoxide. Additionally, ozone caused a modest increase in spontaneous PGD2 
      generation only under cytotoxic conditions. Thus ozone appears to inhibit mast 
      cell degranulation after IgE- or A23187-mediated stimulation and causes direct 
      release of mast cell granule products and PGD2 only under conditions associated 
      with membrane cytotoxicity.
FAU - Peden, D B
AU  - Peden DB
AD  - Department of Pediatrics, School of Medicine, University of North Carolina-Chapel 
      Hill 27599, USA.
FAU - Dailey, L
AU  - Dailey L
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - Am J Physiol
JT  - The American journal of physiology
JID - 0370511
RN  - 37341-29-0 (Immunoglobulin E)
RN  - 37H9VM9WZL (Calcimycin)
RN  - 66H7ZZK23N (Ozone)
RN  - EC 1.11.1.6 (Catalase)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
RN  - RXY07S6CZ2 (Prostaglandin D2)
SB  - IM
MH  - Animals
MH  - Asthma/physiopathology
MH  - Calcimycin/pharmacology
MH  - Catalase/pharmacology
MH  - Cell Line
MH  - Cell Survival/drug effects
MH  - Cytoplasmic Granules/drug effects/physiology/ultrastructure
MH  - Dose-Response Relationship, Drug
MH  - Humans
MH  - Immunoglobulin E/pharmacology/physiology
MH  - Kinetics
MH  - Leukemia, Basophilic, Acute
MH  - Mast Cells/drug effects/*physiology
MH  - Ozone/*pharmacology
MH  - Prostaglandin D2/metabolism
MH  - Rats
MH  - Superoxide Dismutase/pharmacology
MH  - Tumor Cells, Cultured
EDAT- 1995/06/01 00:00
MHDA- 1995/06/01 00:01
CRDT- 1995/06/01 00:00
PHST- 1995/06/01 00:00 [pubmed]
PHST- 1995/06/01 00:01 [medline]
PHST- 1995/06/01 00:00 [entrez]
AID - 10.1152/ajplung.1995.268.6.L902 [doi]
PST - ppublish
SO  - Am J Physiol. 1995 Jun;268(6 Pt 1):L902-10. doi: 10.1152/ajplung.1995.268.6.L902.