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Inadequate reactions of the immune system, i.e. allergic or hypersensitivity reactions, can lead to lung tissue injury. We investigated the relationship of type IV hypersensitivity, as an example of IgE independent hypersensitivity, with the induction of airway hyperreactivity. After antigen challenge (picrylsulphonic acid (PSA] in picrylchloride (PCl) sensitized mice, peribronchial and perivascular accumulation of mononuclear cells was found that was maximal 48 h after challenge. At several time points after challenge, changes in smooth muscle tone of mouse isolated tracheas were measured isometrically. In sensitized mice the response to carbachol was increased, reaching a maximum 48 h after challenge. This hyperreactivity was not found in athymic (nude) mice. We concluded from these data that airway hyperreactivity can be immunologically induced other than by IgE. [ABSTRACT FROM AUTHOR]

Pathological induced changes in beta-adrenoceptor function occur in diseases such as asthma and hypertension. The mechanism(s) of this dysfunction is at present unclear. In the present study, the effect of lymphokines on beta-adrenoceptor agonist induced cAMP production in peripheral blood mononuclear cells (PBMC) is investigated. Pre- incubation of PBMC during 20 h with interleukin-2 (IL-2, 100 u ml-1) and granulocyte/macrophage-colony stimulating factor (GM-CSF, 100 u ml- 1) significantly decreases beta-adrenoceptor agonist induced cAMP production by 35 +/- 8% and 37 +/- 11% respectively. IL-3 and IL-4 do not affect beta-adrenoceptor agonist induced cAMP production in PBMC. It can be concluded that IL-2 and GM-CSF, mediators derived from T- lymphocytes, can induce beta-adrenoceptor dysfunction in PBMC. [ABSTRACT FROM AUTHOR]

The possible role of neutrophils and the endothelium in the induction of hyperreactivity of the pig coronary artery to histamine was studied. In pig isolated coronary arteries histamine caused a concentration- dependent contraction; maximal contraction to histamine, however, was reduced in endothelium-denuded arteries. Pre-incubation of intact coronary arteries with isolated neutrophils did not affect the contractile response to histamine, while pre-incubation of endothelium- denuded arteries induced a hyperreactivity to histamine. This induction of hyperreactivity to histamine by neutrophils in pig coronary arteries seems to be mediated by lipoxygenase products, since it could be prevented by pre-incubation of the preparations with lipoxygenase inhibitors, but not with inhibitors of cyclo-oxygenase or with scavengers. [ABSTRACT FROM AUTHOR]

Guinea pigs were inoculated intra-tracheally with bovine parainfluenza type 3 virus (PI-3) to investigate whether airway hyperreactivity was associated with an increase in the number of broncho-alveolar cells. Two days after saline or PI-3 inoculation no difference in histamine reactivity of the isolated tracheal spirals was observed. The number of broncho-alveolar cells was also not changed. However, 4 days after PI-3 inoculation the histamine-induced contraction of the tracheal spirals was increased by 45% and the number of inflammatory cells in the airways by 150% as compared with the control group. In conclusion, PI-3 infection of the guinea pig respiratory airways induces tracheal hyperreactivity which is associated with an increase in broncho- alveolar cells. [ABSTRACT FROM AUTHOR]