The products of oxygen reduction (superoxide anion, hydrogen peroxide, hydroxyl radicals) and excitation (singlet oxygen) have been implicated in the toxic properties of phagocytes (neutrophils, eosinophils, and mononuclear phagocytes). Enzymes that potentiate (such as peroxidase) or limit (such as catalase, superoxide dismutase) the toxicity of these agents contribute to the complexity of the oxygen-dependent antimicrobial systems of phagocytes. These toxic systems are dormant when the phagocyte is at rest but are activated when the need arises and directed to the destruction of invading microorganisms and other foreign cells. Occasionally, the toxic systems are directed against normal host cells and in this way contribute to the pathogenesis of disease.

Oxygen metabolism and the toxic properties of phagocytes.

Publisher Summary This chapter reviews information on eosinophil structure and function and provide evidence for the eosinophil as an effector cell for killing helrninths and for causing tissue damage in hypersensitivity diseases. The mammalian eosinophil is distinguished by its characteristic granules. The chapter describes specific or secondary granules with an electron-dense core and an electron-radiolucent matrix and two other distinctive types of eosinophil granules as well. While granules with crystalloid cores are characteristic of most mammalian eosinophils—the horse eosinophil is a notable exception—cores have not been observed in lowest vertebrates with the exception of certain teleost fishes and some birds. The evidence reviewed in the chapter indicates that the eosinophil has the ability to kill many species of helminths and likely does so during worm infection. This toxic ability appears to be regulated by several other cells including mast cells, monocytes, and T lymphocytes. It has also been found that an eosinophil-related protein appears to play an undefined role in human reproduction.

The Eosinophilic Leukocyte: Structure and Function

The complete structure of the anterior sensory nervous system of the small nematode C. elegans has been determined by reconstruction from serial section electronmicrographs. There are 58 neurons in the tip of the head. Fifty-two of these are arranged in sensilla. These include six inner labial sensilla, six outer labial sensilla, four cephalic sensilla and two amphids. Each sensillum consists of ciliated sensory neurons ending in a channel enclosed by two non-neuronal cells, the sheath and socket cells. The amphidial channel opens to the outside as does that of the inner labial sensilla so that these probably contain chemoreceptive neurons. The endings of the other sensilla are embedded in the cuticle and may be mechanoreceptive. The cell bodies of all the neurons lie near the nerve ring and their axons project into the ring or into ventral ganglia. One of the ciliated sensory neurons in each of the six inner labial sensilla makes direct chemical synapses onto a muscle making these sensory-motor neurons. The anatomy of four isogenic animals was compared in detail and found to be largely invariant. The anatomy of juveniles is nearly identical to that of the adult, but males have four additional neuron processes.

Electron microscopical reconstruction of the anterior sensory anatomy of the nematode Caenorhabditis elegans.?2UU.

Eosinophils are pleiotropic multifunctional leukocytes involved in initiation and propagation of diverse inflammatory responses, as well as modulators of innate and adaptive immunity. In this review, the biology of eosinophils is summarized, focusing on transcriptional regulation of eosinophil differentiation, characterization of the growing properties of eosinophil granule proteins, surface proteins and pleiotropic mediators, and molecular mechanisms of eosinophil degranulation. New views on the role of eosinophils in homeostatic function are examined, including developmental biology and innate and adaptive immunity (as well as their interaction with mast cells and T cells) and their proposed role in disease processes including infections, asthma, and gastrointestinal disorders. Finally, strategies for targeted therapeutic intervention in eosinophil-mediated mucosal diseases are conceptualized.

https://www.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-2222.2008.02958.x

Eosinophils: Biological Properties and Role in Health and Disease

Publisher Summary Chemo-, thermo-, and hygroreceptors are primary sensory cells, which bear one or several modified cilia whose membranes are specialized to take part in the transduction process. These membranes must be exposed to the stimuli but also be protected against desiccation, mechanical, and other injury. Hence, a variety of structural specializations is found that serves these functions. In insects, chemo-, thermo-, and hygroreceptive sensory cells are located exclusively in sensilla, which are organelles built up by a definite number of characteristic cells. During development, the innermost enveloping cell produces a cuticular sheath (scolopale), which envelops the dendritic processes for varying distances along their course through the receptor lymph cavity. This sheath producing cell is surrounded by the trichogen cell, which is itself surrounded by the trichogen cell. These cells build up shaft and socket, respectively, of the cuticular outer structures during development. The perikarya of all cells of the sensillum are enclosed within the epidermis.

Ultrastructure of invertebrate chemo-, thermo-, and hygroreceptors and its functional significance.

Schistosoma mansoni: changes in the outer membrane of the tegument during development from cercaría to adult worm.

Eosinophils from the peritoneal cavity of normal rats, in the presence of fresh normal rat serum (NRS), adhered to schistosomula of Schistosoma mansoni in vitro and killed the majority of parasites within 18 h. The reaction differed from the previously described antibody-mediated eosinophil adherence to schistosomula which occurs in heat-inactivated immune rat serum (IRS) and where adherence is mediated through Fc receptors. Adherence of eosinophils in fresh NRS was shown to be due to the activation of complement at the schistosomular surface by the alternative pathway, and it was effected through C3 receptors. The ability of eosinophils to kill in Fc-mediated adherence. This enhancement of killer activity may be due to the generation by complement activation of eosinophil chemotactic factors which increase the concentration of cells at the target surface. It is suggested that eosinophil adherence mediated through complement activation could be the principla mechanism of destroying schistosomula in the host.

/pdf/complement-mediated-killing-of-schistosomula-of-schistosoma-3wqanemix2.pdf

Complement-mediated killing of schistosomula of Schistosoma mansoni by rat eosinophils in vitro.

Unusual bodies have been described in the hypodermal tissues of larval Dirofilaria immitis and Brugia pahangi. Ultrastructural evidence indicates that these bodies are probably Gram-negative micro-organisms. It appears that the presence of large numbers of these bodies in an early embryo may affect development adversely. Their importance at later stages of development of filariae is not known.

Micro-organisms in filarial larvae (Nematoda).

SUMMARY
Purified eosinophil and neutrophil cationic proteins isolated from the lysosomal secretion granules of human granulocytes, evoke characteristic, dose-dependent morphological changes in young schistosomula of S. mansoni. The first sign of damage is seen within 15–30 min of incubation and involves the formation of surface microvilli and blebs. Subsequently, tegumental evaginations of varying size are developed, but these appear to explode with rapidity, so that lengths of expanded tegumental outer membrane are deposited over the severely damaged surface of the parasite. Both types of granulocyte proteins are able to effect comparable damage at equimolar concentration. Other cationic proteins such as protamine and poly-L-arginine also damage the parasite surface but the pathological changes differ from those induced by the granulocyte proteins and they take longer to develop. In contrast, lysozyme-treated parasites are virtually similar to control schistosomula incubated in medium alone. These findings are discussed in relation to published data concerning the interaction of intact granulocytes with young schistosomula both in vitro and in viva.

Morphological studies on the killing of schistosomula of Schistosoma mansoni by human eosinophil and neutrophil cationic proteins in vitro.

THE blood fluke Schistosoma mansoni has an unusual tegumental outer membrane which consists of two lipid bilayers1,2. We report here that the double outer membrane is a common feature of the Schistosomatidae (parasites of man which cause schistosomiasis) and also occurs in members of the two other families of blood flukes3, the Aporocotylidae (parasites of fish) and the Spirorchiidae (parasites of turtles). In contrast, flukes (Digenea) belonging to families which inhabit the gut and associated body cavities of the host are limited by a single lipid bilayer. We suggest that the double outer membrane is an adaptation to the intravascular habitat.

Diane J. McLaren

Papers

Schistosoma mansoni: changes in the outer membrane of the tegument during development from cercaría to adult worm.

Complement-mediated killing of schistosomula of Schistosoma mansoni by rat eosinophils in vitro.

Micro-organisms in filarial larvae (Nematoda).

Morphological studies on the killing of schistosomula of Schistosoma mansoni by human eosinophil and neutrophil cationic proteins in vitro.

Blood flukes have a double outer membrane