1. Mechanisms of eosinophil-associated inflammation
Gerald J. Gleich, MD 
Journal of Allergy and Clinical Immunology 
Volume 105, Issue 4, Pages (April 2000)
DOI: /mai
Copyright © 2000 Mosby, Inc. Terms and Conditions

2. Fig. 1
Eosinophil maturation in bone marrow. After allergen-induced late-phase reaction, CD34+ cells express IL-5 receptor α-chain. IL-5 drives the CD34+ and IL-5 receptor α-chain+ cells to eosinophil maturation. Under the stimulus of IL-5 or eotaxin, these mature cells shed L-selectin and migrate from the bone marrow to the blood.
Journal of Allergy and Clinical Immunology  , DOI: ( /mai )
Copyright © 2000 Mosby, Inc. Terms and Conditions

3. Fig. 2
Schematic summary of eosinophil recruitment to and activation in bronchial tissues. At 1 , the eosinophil is moving in the peripheral blood. At 2 , the eosinophil has tethered to the vessel wall by adhesion molecules (for example, endothelial P-selectin and eosinophil very late activation antigen [VLA]-4 with endothelial vascular cell adhesion molecule [VCAM]-1) and rolls along the endothelium. At 3 , the eosinophil has more firmly adhered to the endothelium (by the eosinophil β1- and β2-integrins and the endothelial intercellular cell adhesion [ICAM] molecules) and has flattened on the surface. At 4 , the eosinophil is undergoing transmigration between endothelial cells into the connective tissues. At 5 , the eosinophils (with use of VLA-4 and VLA-6) interact with connective tissue matrix proteins (eg, fibronectin and laminin), become “primed” and partially activated under the influence of various factors (eg, cytokines such as IL-5, chemokines such as RANTES and eotaxin, and lipid mediators such as PAF), and migrate toward their eventual destination. At 6 , eosinophils become fully activated (by interactions with cytokines, lipid mediators, Igs, complement fragments, and β2 integrins) and start to degranulate. Finally, at 7 , the eosinophils have degranulated, releasing toxic mediators (eg, granule proteins, lipid mediators, oxygen metabolites, proteases, and cytokines) and disrupting cells in the bronchial epithelium.
Journal of Allergy and Clinical Immunology  , DOI: ( /mai )
Copyright © 2000 Mosby, Inc. Terms and Conditions

4. Fig. 3
Proposed role of eosinophils in bronchial asthma. Bronchus, top right , shows a normal portion; top left , epithelial damage resulting from toxic eosmophil granule proteins; bottom left , edematous airway with smooth muscle hyperplasia. X , Halide anions, such as Cl–, Br–, or I–. (Modified from Gleich GJ, Adolphson CR. The eosinophil and bronchial asthma: evidence for a critical role of eosinophils in pathophysiology. In: Sanderson CJ, editor. Interleukin-5: from molecule to drug target for asthma. Vol 125. New York: Marcel Dekker; p )
Journal of Allergy and Clinical Immunology  , DOI: ( /mai )
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5. Fig. 4
Interaction among eosinophils, MBP, and M2 muscarinic receptors in the lung. M2 receptors are present on terminals of the vagus nerve. M3 receptors are present on respiratory smooth muscle. Stimulation of the M2 receptor decreases acetylcholine release from terminals of the vagus nerve. Stimulation of M3 receptors causes muscle contraction. Eosinophils selectively infiltrate areas around nerves and degranulate. MBP released from the eosinophil allosterically blocks the M2 receptor, thereby increasing acetylcholine release from the terminals of the vagus nerve.
Journal of Allergy and Clinical Immunology  , DOI: ( /mai )
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6. Fig. 5
Viral titers from the lungs of virus-exposed guinea pigs. Sensitized virus-infected guinea pigs (white bar , n = 19) showed a significant decrease in viral titer compared with nonsensitized virus-infected guinea pigs (black bar , n = 11, P = .04). Pretreatment with antibody to IL-5 had no effect on nonsensitized virus-infected guinea pigs (hatched bar , n = 3) but caused a significant increase in recovered virus from sensitized virus-infected animals (light gray bar , n = 11, P < .0001). Sensitized virus-infected guinea pigs treated with antibody to MBP (dark gray bar , n = 7) continued to show decreased viral titers compared with untreated sensitized virus-infected animals. (Reproduced from Adamko DJ, Yost BL, Gleich GJ, Fryer AD, Jacoby DB. Ovalbumin sensitization changes the inflammatory response to subsequent parainfluenza infection: eosinophils mediate airway hyperresponsiveness, M2 muscarinic receptor dysfunction, and antiviral effects. J Exp Med 1999;190: by copyright permission of the Rockefeller University Press.)
Journal of Allergy and Clinical Immunology  , DOI: ( /mai )
Copyright © 2000 Mosby, Inc. Terms and Conditions