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Defense Reaction (defense + reaction)
Selected AbstractsHuntingtin inclusion bodies are iron-dependent centers of oxidative eventsFEBS JOURNAL, Issue 23 2006Wance J. J. Firdaus Recently, we reported that the transient expression of huntingtin exon1 polypeptide containing polyglutamine tracts of various sizes (httEx1-polyQ) in cell models of Huntington disease generated an oxidative stress whose intensity was CAG repeat expansion-dependent. Here, we have analyzed the intracellular localization of the oxidative events generated by the httEx1-polyQ polypeptides. Analysis of live COS-7 cells as well as neuronal SK-N-SH and PC12 cells incubated with hydroethidine or dichlorofluorescein diacetate revealed oxidation of these probes at the level of the inclusion bodies formed by httEx1-polyQ polypeptides. The intensity and frequency of the oxidative events among the inclusions were CAG repeat expansion-dependent. Electron microscopic analysis of cell sections revealed the presence of oxidation-dependent morphologic alterations in the vicinity of httEx1-polyQ inclusion bodies. Moreover, a high level of oxidized proteins was recovered in partially purified inclusions. We also report that the iron chelator deferroxamine altered the structure, localization and oxidative potential of httEx1-polyQ inclusion bodies. Hence, despite the fact that the formation of inclusion bodies may represent a defense reaction of the cell to eliminate httEx1 mutant polypeptide, this phenomenon appears inherent to the generation of iron-dependent oxidative events that can be deleterious to the cell. [source] Eicosanoids mediate the laminarin-induced nodulation response in larvae of the flesh fly, Neobellieria bullataARCHIVES OF INSECT BIOCHEMISTRY AND PHYSIOLOGY (ELECTRONIC), Issue 1 2005Vanessa Franssens Abstract Insects have a highly developed innate immune system, including humoral and cellular components. The cellular immune responses refer to hemocyte-mediated processes such as phagocytosis, nodulation, and encapsulation. Nodulation is considered the predominant defense reaction to infection in insects. Treating third instar larvae of the grey flesh fly, Neobellieria bullata, with laminarin (,-1,3-glucan, a typical component of fungal cell walls) induced nodulation in a dose-dependent manner. This reaction was initiated very soon after injection and reached its maximal response level after 4 h. The nodules were not randomly distributed in the hemocoel, but were concentrated around the crop. The possible role of eicosanoids in this nodulation process was determined by treating larvae with the phospholipase A2 inhibitor, dexamethasone, the cyclooxygenase inhibitor, naproxen, and the lipoxygenase inhibitor, esculetin. Both dexamethasone and naproxen significantly impaired the ability of N. bullata larvae to form nodules in response to laminarin. Supplying dexamethasone-treated larvae with the eicosanoid precursor, arachidonic acid, restored the full response. On the other hand, treating larvae with esculetin did not influence the formation of nodules in response to laminarin. This is the first study that demonstrates the occurrence of a laminarin-induced nodulation response in Diptera. Phospholipase A2 and cyclooxygenase activities, both involved in prostaglandin biosynthesis, appear to play an important role in the regulation of this process. Arch. Insect Biochem. Physiol. 59:32,41, 2005. © 2005 Wiley-Liss, Inc. [source] Eicosanoids influence in vitro elongation of plasmatocytes from the tobacco hornworm, Manduca sextaARCHIVES OF INSECT BIOCHEMISTRY AND PHYSIOLOGY (ELECTRONIC), Issue 1 2005Jon S. Miller Abstract Nodule formation is the predominant insect cellular defense reaction to bacterial challenges, responsible for clearing the largest proportion of infecting bacteria from hemolymph circulation. Hemocyte spreading behavior is a critical step in the nodulation process. It has been suggested that eicosanoids mediate several steps in the process. However, the influence of eicosanoids on hemocyte spreading has not been investigated in detail. To test the hypothesis that eicosanoids mediate hemocyte spreading behavior, I treated larvae of the tobacco hornworm, Manduca sexta, with eicosanoid biosynthesis inhibitors and later assessed plasmatocyte elongation on glass slides. Plasmatocytes from larvae treated with dexamethasone did not elongate to the extent of plasmatocytes from untreated control larvae. The dexamethasone effect on plasmatocyte elongation was expressed in a dose-dependent manner and was reversed by injecting dexamethasone-treated larvae with the eicosanoid-precursor fatty acid, arachidonic acid. Palmitic acid, which is not substrate for eicosanoid biosynthesis, did not reverse the influence of dexamethasone on plasmatocyte elongation. Finally, plasmatocytes from larvae treated with a range of eicosanoid biosynthesis inhibitors did not elongate to the extent of plasmatocytes from control larvae. Plasmatocyte width did not appear to be influenced in this study. These findings strongly support the idea that insect plasmatocyte elongation is influenced by eicosanoids. Arch. Insect Biochem. Physiol. 59:42,51, 2005. © 2005 Wiley-Liss, Inc. [source] Spanning the gap: experimental determination of paratenic host specificity of horsehair worms (Nematomorpha: Gordiida)INVERTEBRATE BIOLOGY, Issue 1 2003Ben Hanelt Abstract. Details of the life cycle of freshwater nematomorphs (gordiids) remain unclear. Free-living aquatic larval gordiids must make a critical transition from an epibenthic aquatic environment to terrestrial hosts. In order to identify potential hosts capable of bridging this ecological gap, the specificity of paratenic hosts of three common species of North American gordiids was investigated. All three species were characterized by an identical infection pattern: low host specificity. Gordiids were able to encyst within annelids, mollusks, crustaceans, insects and a vertebrate. Three species of putative host (a turbellarian, a water mite, and a mosquito larva) were not infected with any of the gordiid species. Internal defense reactions (IDR) and feeding behaviors are implicated as preventing infection in these species. Several of the other host species produced either an IDR or an immune reaction to the cysts, although reactions to the cysts were highly variable between species. In most species, IDR did not cause noticeable harm to the encysted larvae. It is proposed that although many species are easily infected with gordiid cysts, most do not act as natural paratenic hosts. For some of these host groups, especially snails, a role as reservoir host is suggested. Of all hosts included in this study, aquatic insects were identified as the hosts likely responsible for spanning the ecological gap and acting as true hosts for gordiids. [source] Developmental strategy of the endoparasite Xenos vesparum (strepsiptera, Insecta): Host invasion and elusion of its defense reactionsJOURNAL OF MORPHOLOGY, Issue 7 2007Fabio Manfredini Abstract To successfully complete its endoparasitic development, the strepsipteran Xenos vesparum needs to elude the defense mechanisms of its host, the wasp Polistes dominulus. SEM and TEM observations after artificial infections allow us to outline the steps of this intimate host,parasite association. Triungulins, the mobile 1st instar larvae of this parasite, are able to "softly" overcome structural barriers of the larval wasp (cuticle and epidermis) without any traumatic reaction at the entry site, to reach the hemocoel where they settle. The parasite molts 48 h later to a 2nd instar larva, which moves away from the 1st instar exuvium, molts twice more without ecdysis (a feature unique to Strepsiptera) and pupates, if male, or develops into a neotenic female. Host encapsulation involves the abandoned 1st larval exuvium, but not the living parasite. In contrast to the usual process of encapsulation, it occurs only 48 h after host invasion or later, and without any melanization. In further experiments, first, we verified Xenos vesparum's ability to reinfect an already parasitized wasp larva. Second, 2nd instar larvae implanted in a new host did not evoke any response by hemocytes. Third, we tested the efficiency of host defense mechanisms by implanting nylon filaments in control larval wasps, excluding any effect due the dynamic behavior of a living parasite; within a few minutes, we observed the beginning of a typical melanotic encapsulation plus an initial melanization in the wound site. We conclude that the immune response of the wasp is manipulated by the parasite, which is able to delay and redirect encapsulation towards a pseudo-target, the exuvia of triungulins, and to elude hemocyte attack through an active suppression of the immune defense and/or a passive avoidance of encapsulation by peculiar surface chemical properties. J. Morphol., 2007 © 2007 Wiley-Liss, Inc. [source] | |||||||||||||