Table 1.

Potential mechanisms of virus-induced wheeze (based on ref 1).

Acute inflammation	Increased bronchial responsiveness (BHR)
1. Changes in small airway function	1. Reduced lung function
∗Oedema and wall thickening	∗Airway wall changes
∗Airway obstruction	∗Bronchoconstriction
2. Alteration neural control	2. Increase in cholinergic responsiveness
(evidence mainly in animal models)	∗BHR prevented by atropine
∗Neural reflex	∗Modulation substance P
∗Interference M2 receptor function	3. Induced neurogenic inflammation
∗Sensory C fibres	4. Potentiated cholinergic neurotransmission
∗Disruption of epithelial barrier	∗Increased sensitivity to constrictor agent
∗Reduction neutral endopeptidase	∗Increased maximal response
3. Neutrophil recruitment and activation
∗IL-8 and LTB4 production	Interaction with airway inflammation
4. Monocytes and macrophages	1. Increased response to allergen (Fig. 2)
∗Release acute phase cytokines, e.g. TNF-α	∗Exaggerated early phase reaction
5. Mediators	∗Enhanced late response
∗LTC4 and PGF2	∗Increased allergen penetration
6. Decreased β-adrenergic sensitivity	2. Potentiation inflammatory cascade
∗Granulocytes decreased response isoprenaline	∗Eosinophil recruitment etc. (Fig. 2)
7. Upregulation ICAM-1 receptor	3. Inefficient antiviral response due to type
∗Increased viral adhesion	2 T-cell cytokine predominance (Fig. 1)