[The countermeasure to pollinosis by a web site of Internet].

For the countermeasure to pollinosis, we opened "the web site of pollinosis by allergic group of otorhinolaryngology, Jikei Medical School" and provided the information of pollinosis for patients in the web site of internet from the spring of 1997. In the web site we kept to be informed of the pollen forecast, daily dispersed pollens, and medical information being renewed frequently of prevention and therapy for pollinosis. For the principle of therapy, we adopted the guideline for allergic rhinitis which was produced by Japan Allergic Societies and recommended visitors to get standard therapy for pollinosis. Consequently, the web site was accessed up to 160,000 times by the summer of 1999 and we received 204 medical questions by e-mail and answered to these all mails. We then made a questionnaire study after 3 each pollen seasons and received over 200 answers which showed that our fresh information was useful to decrease symptoms of pollinosis. These results show that information by web site seems to be useful for the countermeasure to pollinosis and will be more important to support medical treatment in hospitals in future.

IL-4 and IL-6 production of bone marrow-derived mast cells is enhanced by treatment with environmental pollutants.

To examine the potential effects of environmental pollutants on the production of cytokines in mast cells, mouse bone marrow-derived mast cells (BMMC) were cultured at various concentrations of diesel exhaust particulates (DEP) or formaldeyhde. Proliferation of BMMC at 0.8, 2 and 4 microg/ml of DEP and 0.5 and 1 microg/ml of formaldehyde did not differ significantly from that of the controls (0 microg/ml) after 72 h culture, with the exception of a significant decrease in proliferation at 5 microg/ml of formaldehyde. Treatment with DEP or formaldehyde alone did not induce interleukin-4 (IL-4) or IL-6 production by BMMC. IL-4 and IL-6 production in BMMC stimulated with A23187 was higher in BMMC treated with low concentrations of DEP than in controls, but no increase was seen in BMMC treated with high DEP. IL-4 and IL-6 production in A23187-stimulated BMMC was significantly increased at 0.5 and 1 microg/ml formaldehyde but decreased at 5 microg/ml formaldehyde. After pretreatment with low DEP or formaldehyde alone for 24h, IL-4 production of BMMC stimulated with A23187 was lower in BMMC treated with low DEP or formaldehyde than in controls. Antigen-induced IL-4 production significantly increased in BMMC treated with 0.4 or 0.8 microg/ml DEP or 0.5 microg/ml formaldehyde, but antigen-induced IL-6 production in BMMC did not increase at low DEP or formaldehyde. Although the enhancement of IL-4 production of BMMC stimulated with A23187 plus DEP was not completely inhibited by 5x10(-4) M 2-mercaptoethanol (2-ME), treatment with 10(-7) M dexamethasone inhibited further IL-4 production. Cytokine production of mast cells is thus shown here for the first time to be modulated by treatment with DEP or formaldehyde. Environmental pollutants such as DEP and formaldehyde may thus affect the immune response via the modulation of cytokine production in mast cells.

Modulated cytokine production from cervical lymph node cells treated with B[a]P and PCB.

To investigate the effects of Benzo[a]pyrene (B[a]P) and polychlorinated biphenyls (PCB) on in vitro cytokine production, we isolated cervical lymph node cells from ovalbumin (OA)-primed mice and the lymph node cells were cultured with various concentrations of B[a]P or PCB in the presence of antigen presenting cells (APC) and OA. B[a]P significantly increased the levels of interleukin-4 (IL-4) and -6(IL-6) in the culture supernatants. However, the levels of interferon-gamma (IFN-gamma) were decreased by treatment with PCB. These findings indicate that in vitro treatment with B[a]P or PCB modulate cytokine production from lymph node cells.

Inhalation of diesel exhaust enhances antigen-specific IgE antibody production in mice.

To examine the effects of diesel exhaust (DE) inhalation on IgE antibody production, BALB/c mice were exposed to 0 (control), 3.0 and 6.0 mg/m3 DE inhalation for 3 weeks. Intranasal sensitization with ovalbumin (OA) three times at intervals of 3 weeks was conducted immediately before, immediately after and 3 weeks after DE inhalation. Body weight and thymus weight for the DE-exposed and control mice were essentially the same but spleen weight in mice exposed to 6 mg/m3 significantly increased. Anti-OA IgE antibody titers in the sera of mice exposed to 6 mg/m3 was significantly higher than the control. Total IgE and anti-OA IgG in sera for DE-exposed and control mice remained basically the same. To investigate cytokine production in mice exposed to 6 mg/m3, spleen cells from DE-exposed and control mice were stimulated with OA in vitro and cytokine production in the culture supernatants was measured by ELISA. In vitro antigen-stimulated interleukin-4 (IL-4) and -10 (IL-10) production in spleen cells of exposed mice significantly increased compared to the control. In vitro interferon (IFN)-gamma production in spleen cells of exposed mice markedly decreased. DE inhalation is thus shown to have adverse effect on antigen-specific IgE antibody production in mice through alteration of the cytokine network.

[Relationship between the morphological changes of Japanese cedar (Cryptomeria japonica) pollen grains and the release of major allergens from the pollen].

Release of major allergens (Cry j 1, Cry j 2) from Japanese cedar (C. japonica) pollen grains treated with high pressure was investigated. C. japonica pollen grains crushed by high pressure treatment using FRENCH Pressure Cell Press released greater amounts of major allergens, particularly Cry j 2, compared to those without crush. This suggests that the cytoplasm of C. japonica pollen grains contains more Cry j 2 than previously reported. The effect of nasal fluid on the release of major allergens from C. japonica pollen grains was analyzed in vitro. Nasal fluid from patients with nasal allergy remarkably increased the release of major allergens from pollen grains, compared to controls, and the amount of Cry j 1 was greater than Cry j 2. Further studies revealed that nasal fluid affects the outer wall of pollen grains, where Cry j 1 is located, to a greater extent than its effect on the cytoplasm, where Cry j 2 is located.

[Comparative study on the assay for IgE antibodies specific for Chamaecyparis obtusa pollen between AlaSTAT and CAP-RAST].

Titers of IgE antibody specific for the pollen of Chamaecyparis obtusa (C. obtusa) were determined by AlaSTAT and CAP-RAST in 221 patients with Japanese cedar pollinosis. IgE antibody to C. obtusa tested positive by CAP-RAST at a higher rate (80.5%) than by AlaSTAT (52.6%). The results obtained from the two assays were compared with those from intradermal skin test. CAP-RAST had a higher sensitivity than that of AlaSTAT. Because the two methods showed no differences in the determination of IgE antibody specific for Cryptomeria japonica, the above differences between AlaSTAT and CAP-RAST are surmised to be ascribable to the differences of C. obtusa antigen used in the both assays.

Intranasal instillation of diesel exhaust particulates and antigen in mice modulated cytokine productions in cervical lymph node cells.

To investigate cytokine production stimulated by diesel exhaust particulates (DEP) and antigen through the intranasal route, mice were administered with DEP mixed with ovalbumin (OA) 3 times at an interval of 3 weeks. After the last instillation, cervical lymph node cells (LNC) were cultured in vitro with OA and antigen-presenting cells. The proliferative response to OA in cervical LNC from mice instilled with DEP and OA was noted to have increased significantly compared to mice instilled with OA alone. Interleukin 4 (IL-4) and interferon (IFN)-gamma in culture supernatants were measured with ELISA. OA-stimulated IL-4 production in cervical LNC from mice instilled with DEP and OA markedly increased beyond that in the control mice. In contrast, OA-stimulated IFN-gamma production in cervical LNC from mice instilled with OA was 3 times that for DEP and OA-instilled mice. OA-specific IgE antibody in sera showed a trend to be increased in mice intranasally instilled with DEP and OA. These results suggest that intranasal instillation of DEP and antigen in mice may modulate in vitro antigen-stimulated cytokine production from cervical LNC with a consequent increase in IgE antibody production.