Pharmacology of the Eosinophil

Lysophosphatidylcholines (lyso-PCs), generated during blood storage, are etiologic in a two-insult, sepsis-based model of transfusion-related acute lung injury (TRALI). Individually, endotoxin (LPS...

https://www.physiology.org/doi/pdf/10.1152/ajpcell.00540.2001

A two-insult in vitro model of PMN-mediated pulmonary endothelial damage: requirements for adherence and chemokine release

PAF. A review of its effects, antagonists and possible future clinical implications (Part II).

1. Exposure of guinea-pigs to aerosols of platelet activating factor (PAF) (0.01 to 100 micrograms ml-1) induced a dose-dependent increased incidence of eosinophils in bronchoalveolar lavage fluid (BAL) at 48 h. Total leucocyte numbers and the percentages of lymphocytes and neutrophils were unchanged in BAL fluid. 2. Increased numbers of eosinophils were detected in BAL 1 h after exposure to PAF but eosinophilia was not maximal until 48 h. One week after exposure to PAF, the percentage of eosinophils in BAL was within the normal range. 3. Depletion of circulating platelets or neutrophils by intravenous injection of specific antisera did not modify accumulation of eosinophils in the airway lumen following inhalation of PAF (10 micrograms ml-1). 4. PAF-induced pulmonary airway eosinophil accumulation was inhibited by treatment with SDZ 64-412, a selective PAF-antagonist, whether the compound was administered before, or 30 min after, inhalation of PAF. 5. Pulmonary airway eosinophil accumulation due to inhaled PAF (10 micrograms ml-1) was inhibited by prior treatment with aminophylline, cromoglycate, ketotifen, dexamethasone and AH 21-132. 6. Pulmonary airway eosinophil accumulation due to inhaled PAF (10 micrograms ml-1) was not inhibited by prior treatment with indomethacin, salbutamol or mepyramine.

/pdf/eosinophil-accumulation-in-pulmonary-airways-of-guinea-pigs-363g834a7w.pdf

Eosinophil accumulation in pulmonary airways of guinea-pigs induced by exposure to an aerosol of platelet-activating factor: effect of anti-asthma drugs.

A mixture of lysophosphatidylcholines (lyso-PCs) are generated during blood storage and are etiologic in models of acute lung injury. We hypothesize that lyso-PCs stimulate polymorphonuclear neutrophils (PMNs) through Ca(2)(+)-dependent signaling. The lyso-PC mix (0.45-14.5 micro M) and the individual lyso-PCs primed formyl-Met-Leu-Phe (fMLP) activation of the oxidase (1.8- to 15.7-fold and 1.7- to 14.8-fold; P<0.05). Labeled lyso-PCs demonstrated a membrane association with PMNs and caused rapid increases in cytosolic Ca(2)(+). Receptor desensitization studies implicated a common receptor or a family of receptors for the observed lyso-PC-mediated changes in PMN priming, and cytosolic Ca(2)(+) functions were pertussis toxin-sensitive. Lyso-PCs caused rapid serine phosphorylation of a 68-kD protein but did not activate mitogen-activated protein kinases or cause changes in tyrosine phosphorylation. With respect to alterations in PMN function, lyso-PCs caused PMN adherence, increased expression of CD11b and the fMLP receptor, reduced chemotaxis, provoked changes in morphology, elicited degranulation, and augmented fMLP-induced azurophilic degranulation (P<0.05). Cytosolic Ca(2)(+) chelation inhibited lyso-PC-mediated priming of the oxidase, CD11b surface expression, changes in PMN morphology, and serine phosphorylation of the 68-kD protein. In conclusion, lyso-PCs affect multiple PMN functions in a Ca(2)(+)-dependent manner that involves the activation of a pertussis toxin-sensitive G-protein.

https://jlb.onlinelibrary.wiley.com/doi/pdf/10.1189/jlb.0402179

Lysophosphatidylcholines prime the NADPH oxidase and stimulate multiple neutrophil functions through changes in cytosolic calcium

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.

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