Administration of diesel exhaust particles (DEP) increases antigen-specific
IgE production and IgE-secreting cells, and induces Th2-type cytokine prof
iles in the airway in mice and humans. To determine the early effects of di
esel exhaust (DE) inhalation on the cytokine production profile, BALB/c mic
e were exposed to 0 (controls) and 1.0 mg/m(3) DE inhalation for 4 weeks. I
ntraperitoneal sensitization with ovalbumin (OVA) was conducted immediately
before DE inhalation. Mice were treated with anti-CD4 or anti-CD8 mAb 1 da
y before and after the sensitization. On day 21, these mice were boosted wi
th OVA and blood; bronchoalveolar lavage (BAL) fluid, and spleens were coll
ected on day 28. In BAL fluid, both TNF alpha and IL-10 production in DE-ex
posed and control mice remained basically the same. IL-6 production in the
anti-CD4 treatment group of DE-exposed mice, however, significantly increas
ed compared with that of the controls. In vitro antigen-stimulated interleu
kin-4 (IL-4) and -1Y (IL-10) production in spleen cells of exposed mice wer
e not affected by low-dose DE inhalation. In vitro interferon (IFN)-gamma p
roduction in the anti-CD4 treated group of exposed mice decreased markedly.
Although anti-OVA IgE production in the plasma of sham-treated mice expose
d to DE was the same level as for controls, anti-CD4 mAb treatment in DE-ex
posed mice significantly reduced IgE production compared to controls. In an
ti-OVA IgG1 production, anti-CD 1 or anti-CD8 mAb treatment in DE-exposed g
roups also significantly reduced. Anti-OVA IgG2a production was reduced by
treatment with anti-CD4, mAb, but increased by anti-CD8 mAb treatment in DE
-exposed mice. Low dose DE inhalation is thus shown to adversely affect the
cytokine and antibody production in mice by altering CD4(+) and CD8(+) T-c
ell functions. (C) 2001 Elsevier Science B.V. All rights reserved.