PubMed · 14178726
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V D KRACUM. 1964. HOW TO EVALUATE YOUR INHALATION THERAPY PROGRAM.. https://pubmed.ncbi.nlm.nih.gov/14178726/
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To examine the hypothesis that Jet Propulsion Fuel (JP-8) inhalation potentiates influenza virus-induced inflammatory responses, we randomly divided female C57BL/6 mice (4-weeks old, weighing approximately 24.6g) into the following groups: air control, JP-8 alone (1023 mg/m(3) of JP-8 for 1h/day for 7 days), A/Hong Kong/8/68 influenza virus (HKV) alone (a 10 microl aliquot of 2000 viral titer in the nasal passages), and a combination of JP-8 with HKV (JP-8 + HKV). The HKV alone group exhibited significantly increased total cell number/granulocyte differential in bronchoalveolar lavage fluid (BALF) compared to controls whereas the JP-8 alone group did not. The JP-8 + HKV group further exacerbated the HKV alone-induced response. However, increases in pulmonary microvascular permeability and pathological alterations in JP-8 + HKV just matched the sum of JP-8 alone- and HKV alone-induced response. Increases in BALF substance P in the JP-8 alone group and BALF leukotriene B4 or total lung compliance in the HKV alone group, respectively were similar to the changes in the JP-8 + HKV group. These findings suggest that changes in the JP-8 + HKV group may be attributed to either JP-8 inhalation or HKV treatment and indicate the different physiological responses to either JP-8 or HKV exposure. Taken together, most of the data did not provide supporting evidence that JP-8 inhalation synergizes influenza virus-induced inflammatory responses.
It is suspected that exposure to low levels of formaldehyde induces or aggravates airway inflammation mediated by immunological and neurological reactions. To clarify the effect of this exposure on allergic inflammatory responses, we exposed female C3H/He mice to 0, 80, 400, or 2000ppb formaldehyde for 12 weeks. When mice were immunized with ovalbumin (OVA) and then exposed to formaldehyde, the numbers of total bronchoalveolar lavage cells, macrophages, and eosinophils in the mice exposed to 2000ppb formaldehyde were significantly increased compared to 0ppb controls. However, the production of interleukin-1beta from bronchoalveolar lavage fluid of these mice decreased significantly. Immunization with OVA significantly increased the production of nerve growth factor, but exposure to 80 and 400ppb formaldehyde significantly reduced the nerve growth factor levels in bronchoalveolar lavage fluid of the immunized mice. In in vitro study, markedly increased lipopolysaccharide-stimulated interferon-gamma production in culture supernatants of spleen cells from 2000ppb formaldehyde-exposed, nonimmunized mice, and significantly increased OVA-stimulated monocyte chemoattractant protein-1 production in culture supernatants of spleen cells from 400 and 2000ppb formaldehyde-exposed, immunized mice were observed. Exposure to 400ppb formaldehyde induced significant decreases in anti-OVA IgG1 and IgG3 antibody productions in plasma, whereas anti-OVA IgE antibody production was not affected. In addition, the levels of nerve growth factor in plasma of 80 and 400ppb formaldehyde-exposed, immunized mice significantly decreased compared to 0ppb control, immunized mice. These results provide the first experimental evidence that low levels of long-term formaldehyde inhalation can induce differential immunogenic and neurogenic responses in allergic mice.
The effect of ozone (O(3)) on the symptoms of allergic asthma and the mechanisms underlying have not yet been fully elucidated. Antigen presentation is one of the factors contributing to the allergic reaction. Therefore, we investigated the effects of repeated exposure to O(3) on antigen-presenting (AP) activity, on the expression of cell-surface molecules associated with antigen presentation (Ia, B7.1, B7.2 and CD11b/c) in bronchoalveolar lavage cells (BAL cells), and on allergic asthma-like symptoms. Rats were exposed to 0.3, 0.56, 1ppm O(3) or filtered air for a 3-day period every 2 weeks, this was replicated three times. AP activity was assessed by measuring antigen-specific T-cell proliferation; and the expression of cell-surface molecules, by flow cytometry. Rats were also made to inhale aerosolized 1% ovalbumin (OVA) or saline for 10min post-exposure to O(3), and allergic asthma-like symptoms were measured by determining the increase in enhanced pause (Penh), which correlates well with lung resistance. O(3) increased both AP activity and expression of Ia and costimulatory molecules in BAL cells concentration dependently. It also increased lung resistance, and the increase in lung resistance after O(3) exposure was significantly higher in the OVA-inhaled group than in the saline-inhaled group. The present results show that O(3) increased AP activity concentration dependently and suggest that O(3) might aggravate allergy symptoms by enhancing AP activity.