Experimental studies in insect parasitism. XVI. The mechanism of the resistance of Nemeritis to defence reactions

1973 ◽  
Vol 183 (1073) ◽  
pp. 337-350 ◽  

The egg of the ichneumon wasp Nemeritis canescens is known to be resistant to the defence reactions of its usual host, Ephestia kuehniella , by virtue of a coating on its surface. The coating is here shown also to endow Nemeritis with resistance to the defence reactions of Achroia grisella and, by implication, several other species of hosts. Three ways in which the coating might act are: (1) passively, by mimicking the lining of the haemocoele; (2) indirectly, by preventing the modification of substances in the haemolymph; (3) directly, by inhibiting the adhesion of blood cells. Mimicry of the host’s internal lining is ruled out by experiments showing that the blood cells of Ephestia react to the internal lining of Achroia , and vice versa, although neither host reacts to Nemeritis . The idea that the coating might prevent modification of substances in the plasma, and so indirectly inhibit encapsulation, is not completely eliminated; but several experiments provide no evidence for it, and several observations favour a hypothesis of direct action by the particles on the blood cells. The nature of that direct action is inconclusively examined. Preliminary experiments suggest that the particles dissociate the cells of young capsules of Ephestia and may, therefore, act to inhibit the adhesion of cells to form capsules. Cells of capsules formed in Tenebrio molitor , which always encapsulates Nemeritis , were not dissociated; which indicates that this mode of action has the required element of specificity. The possibility that substances chemically similar to the particles of Nemeritis might inhibit cell adhesion and aggregation in vertebrates is briefly discussed.

Although caterpillars of Ephestia kuehniella promptly encapsulate alien parasites and other foreign bodies in their haemocoele, they do not normally encapsulate larvae of their habitual parasite Nemeritis canescens , which develop unhindered and eventually destroy their host. The larva of Nemeritis does not achieve this immunity by repelling the blood cells, or by physically dislodging them. It is immune because it is able to live in the haemocoele of Ephestia without evoking a haemocytic reaction; presumably, that is, because it is not recognized as a foreign body. That ability is due to a property of its surface. So long as its surface remains unaltered, the larva, alive or dead, evokes no haemocytic reaction. When its surface is altered whether by perforation, abrasion, or chemical treatment, the living larva evokes a haemocytic reaction in Ephestia and becomes encapsulated. The protective property of its surface is acquired by the larva very late in its embryonic development, between 62 and 66 hours of age at 25 °C. This is about the same time as, or a little later than, the cuticle of the embryonic larva becomes impermeable to water. Four fat solvents were found to deprive the living larva of its immunity, but they may have affected the protective surface by disrupting the underlying wax layer of the epicuticle. Treatments and substances that did not affect the protective surface give some crude indications of its properties, but its ultimate characterization must be in terms of insect immunology. Observations incidental to the main theme of the paper show that the cuticle of the larva is impermeable to water; that ionic exchange takes place through the anus and wall of the rectum, where some food substances may also be absorbed from the blood of the host; and that the order of formation of the cuticulin and wax layers of the embryonic larva is the same as that in ecdysis from instar to instar in other insects. They also provide information on the longevity of bitten supernumerary larvae.


Caterpillars of Ephestia kuehniella promptly encapsulate alien parasites, living tissues from other species of insects, and filaments of such inert substances as Polythene and Polyfluorocarbon implanted in their haemocoele. They do not encapsulate eggs of their habitual parasite Nemeritis canescens , and the paper records an investigation of that failure. Eggs of Nemeritis do not repel the haemocytes or prevent them from forming capsule tissue; they escape encapsulation because they do not stimulate the blood cells to react. The property that enables them to avoid evoking a reaction is located on their surface: dead eggs that retained an unaltered surface were not encapsulated, living or dead eggs of which the surface was experimentally altered were encapsulated. Since eggs of Nemeritis possess this protective surface immediately after oviposition, its origin was sought in the adult parasite . The surface of eggs removed from the distal part of the ovarioles is formed by the chorion; eggs removed from the genital tract below the calyx were found to have a visible layer outside the chorion. When eggs bearing this visible layer were removed from several parts of the genital tract and injected into caterpillars of Ephestia , they were not encapsulated. When eggs not bearing the visible layer outside the chorion were removed from ovarioles, and were injected into caterpillars, they always evoked a haemocytic reaction and were usually completely encapsulated. The property of its surface that enables the egg of Nemeritis to avoid evoking a haemocytic reaction in Ephestia is therefore acquired in the region of the calyx, where also the visible layer appears on the outer surface of the chorion. A few by-products of the investigation are mentioned in the discussion.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Marjan Talebi ◽  
Mohsen Talebi ◽  
Tahereh Farkhondeh ◽  
Jesus Simal-Gandara ◽  
Dalia M. Kopustinskiene ◽  
...  

AbstractChrysin has been shown to exert several beneficial pharmacological activities. Chrysin has anti-cancer, anti-viral, anti-diabetic, neuroprotective, cardioprotective, hepatoprotective, and renoprotective as well as gastrointestinal, respiratory, reproductive, ocular, and skin protective effects through modulating signaling pathway involved in apoptosis, oxidative stress, and inflammation. In the current review, we discussed the emerging cellular and molecular mechanisms underlying therapeutic indications of chrysin in various cancers. Online databases comprising Scopus, PubMed, Embase, ProQuest, Science Direct, Web of Science, and the search engine Google Scholar were searched for available and eligible research articles. The search was conducted by using MeSH terms and keywords in title, abstract, and keywords. In conclusion, experimental studies indicated that chrysin could ameliorate cancers of the breast, gastrointestinal tract, liver and hepatocytes, bladder, male and female reproductive systems, choroid, respiratory tract, thyroid, skin, eye, brain, blood cells, leukemia, osteoblast, and lymph. However, more studies are needed to enhance the bioavailability of chrysin and evaluate this agent in clinical trial studies. Graphic abstract


1956 ◽  
Vol 104 (4) ◽  
pp. 517-523 ◽  
Author(s):  
Joseph C. Turner ◽  

Removal of the white cells and platelets from suspensions of red cells usually produces substantial reduction in the hemolytic activity of venoms. Guinea pig red cells constitute a notable exception and may be lysed by a direct action of venom. White blood cells and platelets appear to contribute to hemolysis by serving as sources of phosphatides for the formation of lysophosphatides. No correlation could be found between phospholipase activity and direct hemolytic activity of venoms. A recently described method (8) of paper chromatographic separation of phospholipides has been used successfully in part of the work.


2017 ◽  
Vol 112 (3) ◽  
pp. 330a
Author(s):  
Ulrich S. Schwarz ◽  
Friedrich Frischknecht ◽  
Michael Lanzer ◽  
Anna Battista ◽  
Christine Lansche ◽  
...  

Parasitology ◽  
1974 ◽  
Vol 68 (2) ◽  
pp. 193-205 ◽  
Author(s):  
P. Götz ◽  
A. Vey

Humoral encapsulation is an effective defence reaction against fungal pathogens. The development of injected spores in the haemocoele of Chironomus larvae may be completely (Aspergillus niger) or partially (Mucor hiemalis) prevented by this reaction. The encapsulation proceeds very rapidly; within 5 min of injection most of the spores are enclosed in a solid capsule. Disintegrating blood cells may participate in the formation of capsule substance, but this is not usually the case. Encapsulation also occurs within the cuticle against invading hyphae of Beauveria bassiana. Histochemical tests show that the capsule substance does not consist of polysaccharides; some tests for proteins and all tests for melanin were positive. The significance of melanin formation and the biochemistry of the phenoloxidase system in insects is discussed in detail. The data presented lead to the conclusion that humoral encapsulation is based upon an activation of phenoloxidases and that the capsule substance represents a polyphenol—protein complex. In contrast to current opinion, the formation of melanin in cellular as well as in humoral encapsulation is not considered to be a secondary process, independent of the actual encapsulation procedure. Instead, the authors interpret the presence of melanin as an indication of the activity of phenoloxidases which cause the formation of a capsule substance on the surface of the parasites.


Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 902-902 ◽  
Author(s):  
Dhananjay K. Kaul ◽  
Sandra M. Suzuka ◽  
Mary Fabry

Abstract Abstract 902 Multiple adhesion molecules, expressed on sickle red blood cells (SS RBCs) and activated endothelium, have been implicated in SS RBC adhesion to vascular endothelium. Moreover, intrinsic differences among heterogeneous SS RBC subpopulations, involving differences in red cell adhesion molecules and cell deformability, may contribute to their adhesive and obstructive properties and lead to postcapillary obstruction. However, the role of SS RBCs in endothelium activation and adhesion has not been evaluated despite the insightful studies of Hebbel and coworkers (JCI, 1982) demonstrating that SS RBCs generate excessive amounts of reactive oxygen species due to the presence of unstable hemoglobin S (HbS) and autoxidation of iron in heme. RBCs from transgenic-knockout sickle (BERK) mice similarly show a pronounced increase in heme degradation (Nagababu et. al. Blood Cells Mol Dis, 2008). We hypothesize that hypoxic conditions in venules (oxygen tension,∼30 mm Hg) will accelerate autoxidation of RBC membrane-bound HbS and release H2O2 that will be transferred to adjoining endothelium resulting in its activation (i.e., up-regulation of endothelial adhesion molecules) and SS RBC adhesion. To test the hypothesis that HbS-containing red cells from BERK mice will result in activation of quiescent endothelium in normal mice, we infused FITC (fluorescein isothiocynate)-labeled BERK red cells into congenic C57BL mice. BERK mice, expressing exclusively human βS- and α-globins, have been extensively backcrossed onto C57BL background. Intravital observations were made in the cremaster muscle microcirculatory bed. A single bolus of 150 μl of FITC-labeled BERK RBCs (Hct 30%) was infused into the recipient C57BL mouse via the jugular vein over a period of 5 min to avoid any shear related platelet aggregation. Infusion of FITC-labeled control (C57BL) mouse RBCs into C57BL recipient mice resulted in rare or no RBC adhesion, suggesting that there was no activating effect on endothelium. In contrast, infusion of BERK mouse RBCs into C57BL mice resulted in time-dependent increase in adhesion to venular endothelium. Adhesion became discernable after 3 minutes and showed a 3-5 fold increase after 5-min compared with the number of adherent RBCs at 3 min (P<0.01). Next, we investigated if the infusion of BERK mouse RBCs would induce increased endothelial oxidants. To this end, the cremaster preparation was suffused for 15 min with 123 dihydrorhodamine (DHR), a H2O2-sensitive probe (10 μl/L), followed by a bolus infusion of BERK mouse RBCs, and time-dependent changes in DHR fluorescence intensity were monitored in venules, the sites of adhesion. Infusion of BERK mouse RBCs, but not C57BL RBCs, resulted in time-dependent increase in the fluorescence intensity (ΔI) in venular endothelium, with almost 5-fold increase in DHR intensity after 5 min of BERK RBC infusion (P<0.001) compared with ΔI at 1 min. When infusion of catalase (900 U/mouse) into recipient C57BL mice was followed 30 min later by a bolus of FITC-labeled BERK mouse RBCs, BERK RBC adhesion and pronounced DHR fluorescence in endothelium were observed, demonstrating that intravascular infusion of catalase had little effect on oxidant generation by BERK mouse RBCs. In contrast, infusion of BERK RBCs pre-treated with catalase (100 U in 0.2 ml RBC suspension, 9-fold less catalase per mouse) to quench RBC generated H2O2 inhibited endothelial DHR fluorescence and BERK RBC adhesion. These results strongly suggest an obligatory role of heme-mediated peroxide generation by SS RBC in endothelial activation and SS RBC adhesion, and support the notion that heme-mediated oxidant generation may play a vital role in endothelial dysfunction in sickle cell disease. Disclosures: No relevant conflicts of interest to declare.


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