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EC number: 271-089-3
CAS number: 68515-47-9
Bronchial asthma is mediated, in part, by the immunoregulatory cytokines
interleukins 4 and 13 (IL-4 and IL-13). These cytokines stimulate IgE
synthesis that in turn is associated with airway hyper-responsiveness.
Compounds that stimulate IgE synthesis and elicit bronchial reactivity
are generally considered to be respiratory sensitizers. To address this
question, topical application (and challenge) of test substances (DINP
included) to mice followed by measurements of total serum IgE was
performed. In addition, auricular lymph nodes were harvested for
measurement of IL-4 and IL-13 proteins and their corresponding messenger
RNAs. Because skin absorption of high molecular weight phthalates is
limited, liver weight increase, a measure of peroxisomal proliferation,
was monitored to assure that internal dosing had been achieved. ELISA
and RNAse protection assays demonstrated that DINP treatment did not
significantly affect IgE, IL-4, or IL-13 levels. Similarly, IL-4 and
IL-13 mRNA levels were not elevated. In contrast, all of these were
significantly elevated by trimellitic anhydride (TMA), a respiratory
sensitizer used as the positive control in this assay. Another control,
dinitrochlorobenzene (DNCB), a contact sensitizer, also responded as
expected, producing smaller but statistically significant increases in
IgE and in mRNA for IL-4 and IL-13 but not in the levels of these
cytokines. In summary, treatment with DINP did not result in significant
elevations indicating that DINP has little, if any, potential to produce
anti-body-mediated respiratory allergy.
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