Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 4 de 4
Filter
Add more filters










Database
Language
Publication year range
1.
Parazitologiia ; 37(5): 428-35, 2003.
Article in Russian | MEDLINE | ID: mdl-14658314

ABSTRACT

Since investigations of Fisher and Sanborn (1964), the most popular point of view on pathological alterations in the development of insects is the statement that microsporidians can produce and secrete the insect juvenile hormone in infected tissues. We suppose that the juvenilizing effect of microsoporidian infection may be a consequence of stress induced by the protozoan invasion. To our opinion, microsporidians can not be a source of juvenile hormone in parasitized insects because of several reasons. 1. The juvenilizing effect of infection may be explained by other reason, that is the stress effect of invasion. 2. Until now nobody can find juvenile hormone in microsporidians. 3. An increase of juvenile hormone titre either alters non-metabolic activity of fat body or alters it in a way that is not favorable for microsporidias. 4. Some effects of the microsporidian infection more resemble an action of ecdysone, but not juvenile hormone. Hypothesis of parasitic stress can explain this, while hypothesis of production JH by microsporidians can not. 5. An effect of invasion by parasites of other systematic groups onto the hormone balance is of the same type. But nobody thinks that other parasites can produce juvenile hormone. Nevertheless it is clear that a high titre of the juvenile hormone is favorable for the microsporidian infection in larvae, especially the last instars. The most descriptions of microsporidian infections are related with this age of insects. Juvenilizing effect of Nosema implantant in the work of Fisher and Sanborn (1964) may be easily explained by decreasing of JH-esterase activity. But in this case the decrease of JH-esterase activity after the implantation of infected tissue in a healthy insect should be explained. We suppose that this fact witness the existence of stress-factor produced by damaged cells of fat body that can enter the healthy cells of fat body and inhibit the activity of JH-esterases.


Subject(s)
Hormones/metabolism , Host-Parasite Interactions/physiology , Insecta/parasitology , Microsporidia/physiology , Animals , Juvenile Hormones/metabolism , Microsporidia/pathogenicity
2.
Parazitologiia ; 37(4): 316-23, 2003.
Article in Russian | MEDLINE | ID: mdl-14515509

ABSTRACT

Pathological alterations being similar to those that can be seen while hormonal dysbalance, particularly the increase of juvenile hormone (JH) titre, is one of the consequences of microsporidian infections. Though the increase of JH in insects infected with microsporidia has not been shown directly, there are many indirect proofs of this. It has been believed that JH is produced by microsporidia. But this has not been shown for microsporidia or for other endoparasites. In this article we want to propose another hypothesis. We suppose that during microsporidiosis the following events develop: exhaustion of host nutrition stores and other destructive consequences of microsporidian dwelling in host cells lead to the decrease of host biosynthetical and reparation activity in the infected cells and then to destructive alterations that can be seen by electro-microscopic methods. The infected cells are stressed and then the typical answer for many physiological stresses follows. Secretion of prothoracicotropic hormone by brain neurosecretory cells is inhibited and as a result the production and release of ecdysone is also inhibited and ecdysteroid titre decreases. The activity of JH-esterases is decreased and as a result the JH titre is increased. If microsporidian infection causes the stress in the host cells, the endocrine system will undoubtedly answer to this stress and this answer will definitely be the same as for all other stresses. Thus, in any case JH titre will be increased in infected insects independently of whether microsporidia produce JH or not. So, hormonal alterations in infected insects should be the consequence not of the microsporidian JH production but of the host response reaction to infection. We suppose that microsporidia do not differ from other parasites of insects and that they can not produce JH.


Subject(s)
Insecta/physiology , Insecta/parasitology , Microsporidia , Animals , Brain/metabolism , Ecdysteroids/metabolism , Insect Hormones/metabolism , Insecta/enzymology , Juvenile Hormones/metabolism
4.
Tsitologiia ; 45(8): 826-31, 2003.
Article in Russian | MEDLINE | ID: mdl-15216635

ABSTRACT

At present a concept prevails that pathological alterations in insect hosts infected with microsporidia, and those associated with hormone imbalance may be explained by the production of juvenile hormone-like (JH) substances by microsporidia. According to another view point, this pathology is a consequence of the host response. We suggested that the microsporidian infection can provoke a stress reaction in insects, which may cause JH secretion by these insects. To confirm this hypothesis, we have analysed major stress protein Hsp70 levels in the infected insects. Using affinity chromatography on ATP-agarose and immunoblotting, we have shown that Hsp70 was accumulated in infected crickets, and that it was the host protein. The consequence of events accompanying the infection in the insects is discussed in relation to the response of hormonal system of the host organism.


Subject(s)
Fat Body/metabolism , Gryllidae/physiology , Gryllidae/parasitology , HSP70 Heat-Shock Proteins/metabolism , Microsporidia/physiology , Animals , Chromatography, Affinity , Corpora Allata/metabolism , Fat Body/parasitology , Gryllidae/anatomy & histology , HSP70 Heat-Shock Proteins/blood , Hemolymph/chemistry , Host-Parasite Interactions , Juvenile Hormones/metabolism , Microsporidia/pathogenicity , Microsporidia/ultrastructure
SELECTION OF CITATIONS
SEARCH DETAIL
...