Many different mediators have been implicated in allergic responses and allergic diseases.14 It is becoming increasingly apparent that no single mediator can account for allergic diseases, such as asthma, rhinitis, eczema, or anaphylaxis, and that the clinical manifestation depends on a complex interaction of mediators that are released from a variety of cells. Although previous research concentrated on the mast cell as the key cell in allergic reactions, it now appears likely that other inflammatory cells, such as macrophages, eosinophils , neutrophils, platelets, and lymphocytes, may also contribute to the inflammatory response. The recognition that cells, other than mast cells, such as eosinophils,5 platelets,6 and macrophages,7 may be activated by IgE-dependent mechanisms has focused attention on these other cells as sources of mediators. Histamine,8 prostaglandinsg and leukotrienes3 have been previously proposed as playing a role in mediating allergic responses. Another mediator that is receiving increasing attention is PAF, a highly potent inflammatory mediator formed, like prostaglandins and leukotrienes, by the action of phospholipase A, on membrane phospholipids. The purpose of this article is to review the various effecs of PAF that may be relevant to allergic diseases and to speculate on its possible involvement in allergy. With the introduction of specific PAF antagonists during the next few years, the role of this inflammatory mediator will be clarified. had previously been demonstrated in the rabbit that platelets provided the major source of histamine among the blood elements,” but it was not known whether histamine release during allergen challenge represented a direct or indirect consequence of the recognition of allergen by antibody. Histamine release in sensitized rabbits undergoing antigen challenge was demonstrated to be the consequence of IgE-dependent activation of basophils that, in turn, released a soluble product capable of eliciting platelet activation.““S ‘* This product was termed PAF and was subsequently demonstrated to be a phospholipid.‘3 The chemical structure was then identified in 1979 by three independent groups as 1-o-alkyl-2-acetyl-sn-glyceryl-3phosphorylcholine (Fig. 1). 14-16 This phospholipid has been variously referred to as PAF-acether,14 acetyl glyceryl ether phosphorylcholine,‘5 or antihypertensive polar renomedullary lipid.16 The original nomenclature (PAF) will be used throughout this article, although it is now apparent that PAF has many other actions in addition to activation of platelets.

https://www.jacionline.org/article/0091-6749(88)90952-9/pdf

Platelet-activating factor as a mediator of allergic disease

Intratracheal administration of platelet-activating factor (paf-acether) induced transient bronchoconstriction in baboons. Using an automated isotopic monitoring system, we found that intratracheal administration of paf-acether also elicited transient accumulation of platelets labeled with 111In oxine within the pulmonary vasculature after the increase in maximal peak inspiratory pressure. Bronchoalveolar eosinophilia was evident 1 h after challenge. The increases in peak inspiratory pressure and bronchoalveolar eosinophilia were inhibited by prophylactic administration of the antiasthma drug ketotifen but not by pyribenzamine, suggesting that the effects of ketotifen are unrelated to H-1 receptor antagonism. Platelet accumulation was not affected by ketotifen or pyribenzamine. This study suggests that paf-acether may be a mediator of the eosinophil recruitment in bronchial asthma and that inhibition of this phenomenon by ketotifen may contribute to the therapeutic efficacy of this drug.

Accumulation of platelets and eosinophils in baboon lung after paf-acether challenge. Inhibition by ketotifen.

In mammals, three major oxygenases, cyclooxygenases (COXs), lipoxygenases (LOXs), and cytochrome P450 (CYP450), generate an assortment of unique lipid mediators (oxylipins) from polyunsaturated fatty acids (PUFAs) which exhibit pro- or anti-thrombotic activity Over the years, novel oxylipins generated from the interplay of theoxygenase activity in various cells, such as the specialized pro-resolving mediators (SPMs), have been identified and investigated in inflammatory disease models Although platelets have been implicated in inflammation, the role and mechanism of these SPMs produced from immune cells on platelet function are still unclear This review highlights the burgeoning classes of oxylipins that have been found to regulate platelet function; however, their mechanism of action still remains to be elucidated

/pdf/the-expansive-role-of-oxylipins-on-platelet-biology-1jbt4xyale.pdf

The expansive role of oxylipins on platelet biology

Platelets have been shown to be important in inflammation, but their role in chronic allergic dermatitis remains unclear. To investigate the role of platelets in a mouse model of chronic contact hypersensitivity induced by repeated elicitation, mice were sensitized and repeatedly elicited in ears with hapten, with or without platelet depletion, by administering antiplatelet antibody or busulfan. Ear thickness, leukocyte infiltration, serum IgE, and scratching behavior significantly decreased in thrombocytopenic mice. cDNA microarray of ear tissue showed reduced gene expression associated with Th2 lymphocytes. Flow cytometry showed increased P-selectin expression on platelets and an increased number of platelet-leukocyte aggregates in blood of repeatedly elicited mice, compared with sham-sensitized mice. In thrombocytopenic mice, inflammation was restored by platelet infusion, which was blocked by platelets from P-selectin-deficient mice or by pretreating platelets with anti-P-selectin antibody. Moreover, injection of activated platelet supernatant into ears led to increased leukocyte infiltration, which was blocked by pretreating platelets with antiplatelet compounds or neutralizing several chemokines in the platelet supernatant. These results suggest that platelets induce leukocyte recruitment into skin by forming platelet-leukocyte aggregates via P-selectin in blood and secreting chemokines at inflamed sites. Therefore, controlling platelet activity may be useful for treatment of chronic allergic dermatitis.

The Role of Platelets in Leukocyte Recruitment in Chronic Contact Hypersensitivity Induced by Repeated Elicitation

Platelet activation and allergic asthma.

Platelet activation in antigen-induced bronchoconstriction.

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Platelet activation in antigen-induced bronchoconstriction.