Allergic Pathophysiology of Bovine Lung

Abstract

In mammals in general (including cattle), lung from sensitised subjects liberates histamine and slow-reacting substance of anaphylaxis (SRS-A) as principal primary mediators upon challenge with specific antigen. Additionally, other mediators such as leucotactic factors, kinins and prostaglandins are produced. The principal sources of these inflammatory chemicals are mast cells and leucocytes. In ruminants, in addition to the abovementioned substances, 5-hydroxytryptamine (serotonin, 5HT) and dopamine are evolved.

The pulmonary inflammatory response so induced is subject to intricate systems of checks and balances (feedback-modulation) caused by:

• 1) autonomic neurohormones such as acetylcholine, adrenaline and noradrenaline, by corticosteroids, each liberated locally or systemically as a result of trauma, and by

• 2) local and systemic actions of the chemical mediators themselves.

Modulation of the allergic inflammatory response of cattle is radically different from that in other mammals. In the latter β-sympathomimetics inhibit mediator release whereas α-sympathomimetics and cholinergic agonists cause enhancement. In cattle all sympathomimetic drugs (α and β) inhibit, whereas dopamine enhances mediator release from lung. Paradoxically all sympathomimetics except dopamine enhance histamine release from bovine leucocytes. Dopamine and carbachol are without effect. Histamine itself inhibits histamine release, as does serotonin.

It may be that catecholamines, while directly inhibiting lung histamine release, simultaneously increase leucocyte histamine release. Thus the leucocyte, being a uniquely mobile cell, may operate a negative histamine ‘feedback’ ie reducing further mediator release from tissues. It is possible that during allergic inflammation histamine acts (typically) as a mediator of inflammation, the severity of which might be rendered self-limiting as with increasing concentration, histamine became inhibitory in action. Therefore, the use of antihistaminic drugs might prove to be not merely ineffectual but potentially detrimental.

Further research is required to elucidate more clearly the mechanisms described.