287 Enhanced basophil histamine release (HR) following in vitro incubation with live influenza a virus is attenuated by T-cell depletion

Huftel, M.A.; Swenson, Cheri A.; Borcherding, Wayne; Dick, Elliot C.; Hong, Rosa; Busse, W.

doi:10.1016/0091-6749(91)91570-j

Cited by 2 publications

(2 citation statements)

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“…Interferon An early study by Ida [22] suggested that interferon may be an important factor mediating viral enhancement of histamine release after immunological stimulus. This work was corroborated by Chonmaitree [23] and extended by Busse, who showed that T-cell depletion attenuated the enhanced histamine release from peripheral blood mononuclear cells following incubation with influenza A [24], but that interferon did not alter histamine release after non-immunological stimulation [21]. Viral infections and interferon have also both been shown to increase the biosynthesis of prostaglandins in the macrophage [35].…”

Section: Release Of Inflammatory Mediatorsmentioning

confidence: 75%

“…Hi.stamine Several studies have demonstrated that histamine release from leucocytes (including basophils and mast cells), following immunological and non-immunological stimuli, is increased by infection or incubation with a variety of respiratory viruses including influenza A, rhinovirus parainfluenza virus and RSV [21][22][23][24][25][26][27][28][29][30][31], Recent work with parainfluenza viruses in Brown Norway rats [32] has demonstrated increased release of histamine coupled to a virus-induced increase in bronchiolar mast cells.…”

Section: Release Of Inflammatory Mediatorsmentioning

confidence: 99%

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Viruses as precipitants of asthma symptoms II. Physiology and mechanisms

Bardin¹,

Johnston²,

Pattemore

1992

Clin Experimental Allergy

121

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The upper and lower airways have complimentary roles in the ultimate object of supplying the body with oxygen whilst removing waste products of metabolism. Pathology in one area may trigger a response in another, the physiology of which, in the case of virus-induced asthma exacerbations remains poorly characterized. Viral infection of the upper airways by common cold viruses frequently triggers a response in the lower airways leading to prolonged morbidity, especially in subjects with significant pre-existing airway disease. The induction or amplification of BHR may be an important mechanism whereby asthmatic symptoms are produced although the cellular and tissue events or reflex mechanisms activated by viral illnesses and underlying BHR changes are poorly defined and may be dependent on the type and the severity of infection. Children and asthmatics tend to develop frequent colds setting in motion a sequence of events culminating in airway obstruction and symptoms of wheezing, coughing and chest tightness. This may reflect independent inflammatory changes caused by a simply additive effect of viral damage to the mucosa superimposed upon pre-existing allergic inflammation (Fig. 1). Few if any symptoms will develop in normal subjects with a mild cold whereas significant symptoms may ensue if the cold is severe and induces marked lower airway swelling, secretions and smooth muscle contraction; pathology to which children who have small calibre airways may be particularly susceptible. In asthmatics even a mild cold frequently induces exacerbation of symptoms, while serious life-threatening asthma attacks may occur associated with a severe cold. Some studies have suggested that this effect is not only additive but also synergistic and brought about by release of the mediators already present in increased quantities, the induction of IgE synthesis, or by the potentiation of neural and epithelial damage. The combined effect of both asthma and viruses may thus be amplified and result in a sustained and refractory period of airway obstruction, severe symptoms and unstable asthma. As most hospital admissions for asthma occur over the winter months and soon after the start of the school terms [115], spread of viruses through the community to susceptible individuals may be the single most important cause of sustained exacerbations of asthma. Definition of the pathological and physiological mechanisms involved will lead to better understanding and may thus provide a basis for prevention and the development of effective forms of treatment for virus-induced asthma.

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