PubMed · 4574036
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M Sabathie. [Problems and false problems of impossible artificial ventilation].. https://pubmed.ncbi.nlm.nih.gov/4574036/
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Inhalation of Aspergillus fumigatus, a ubiquitous fungus, results in the development of allergic bronchopulmonary aspergillosis, a disabling allergic lung disease. For better patient management early diagnosis is essential, and understanding of the immune mechanism is important in achieving this goal. Although animal model studies have contributed to the understanding of the disease mechanism, details on the immunopathogenesis are still lacking. In the present study, we have developed an allergic aspergillosis model in wild-type and IL-4 knockout mice and studied the immune and airway responses. The results indicate that the immune response, pulmonary pathology, and airway reactivity comparable to allergic bronchopulmonary aspergillosis are reproducible in wild mice. IL-4 knockout mice showed similar pulmonary pathology, but no increase in airway resistance, suggesting that IgE and hence IL-4 may be important in eliciting the airway response, while other factors may be involved in the inflammatory process.
Sensitization to latex proteins can cause immediate IgE mast cell-mediated reactions. Health care workers have been found to be particularly at risk because of high exposure. Latex allergy can be produced in mice as demonstrated by IgE and eosinophil responses. Thus the mouse is a potential animal model for studying this disease, but the airway response to latex sensitization in mice has not been evaluated previously. In the present study, we immunized BALB/c mice intranasally with nonammoniated latex proteins. Animals were anesthetized, and lung mechanics were evaluated plethysmographically. Changes in pulmonary conductance (GL) and compliance (Cdyn) were measured in response to a nonspecific challenge with methacholine or to a direct challenge with intravenous latex antigen. Latex sensitization resulted in elevated levels of IgE and latex-specific IgG1 as well as interstitial infiltrates consistent with an allergic response. The methacholine dose-response ED50 for GL was 116.4 microg for the control mice and fell significantly to 20.9 microg for latex-sensitized mice. The ED50 calculated for Cdyn was also significantly lower after latex sensitization. The GL in latex-sensitized mice challenged with latex antigen fell significantly from a prechallenge value of 1.87 +/- 0.41 (S.E.) to 0. 198 +/- 0.03 ml x s-1 x cmH2O after latex antigen challenge. The results indicate that latex-sensitized mice did exhibit increased airway reactivity in the methacholine challenge test. The latex allergic response in mice is unique in that direct challenge with latex antigen itself also resulted in a significant airway response.
Bradykinin has an important role in asthma pathogenesis, but its site of action is unclear. It was previously reported by the authors that bradykinin causes a dose-dependent reduction in dynamic compliance but little change in total lung resistance. This suggested that bradykinin may have a preferential effect in the distant lung. The purpose of the current investigation was to better characterize the effects of bradykinin on pulmonary resistance in rodents and explore the role of nitric oxide release in modulating the effect of bradykinin. Airway constriction was induced in the rats by aerosol administration of bradykinin with or without treatments with the inhaled bradykinin-2 receptor antagonist, Hoe 140 or the nitric oxide synthase inhibitors N(G)-nitro-L-arginine methylester or N(G)-monomethyl-L-arginine. Total lung resistance was partitioned into tissue and airway resistance by using the alveolar capsule method. Bradykinin induced a significant increase in both resistances. Hoe 140 abolished the response to bradykinin. The nitric oxide synthase inhibitors enhanced the bronchoconstricting response. In conclusion, the bradykinin response in the rats was not only localized to conducting airways but also involved a relatively selective tissue reaction. Bradykinin-induced bronchospasm in the rat is solely due to activation of bradykinin-2 receptor. Further, it was shown that nitric oxide significantly modulates the bronchospasm caused by bradykinin, suggesting that nitric oxide is an important modulator of airways responsiveness to bradykinin.