Neuroimmunoendocrine modulation in the host by helminth parasites: a novel form of host-parasite coevolution?
Helminth parasites have evolved diverse molecular mechanisms that facilitate their establishment, growth and reproduction inside an immunologically hostile environment. Thus, the physiological interactions during the course of the immune response to helminths are complex. Infection induces antigen-specific recognition by the immune system, which is consequently charged with the responsibility of marshalling the appropriate effector responses necessary to destroy the parasite, or at the very least inhibit its progression. Obviously, the immune system should accomplish this task while minimizing collateral damage to the host. As our understanding of the neuroendocrine system grows, it has become increasingly clear that this complex network of neurotransmitters, hormones, and cytokines plays an important role in mediating immunity. Helminths present an especially complex relationship between pathogen and these physiological systems, with hormonally dependent host factors such as sex and age correlated with parasite success. On top of the effect that this particular type of parasites may have on the invaded host, recent experimental evidence suggests that helminth parasites not only actively evade immune response, but are also able to exploit the hormonal microenvironment within their host to favor their establishment, growth and reproduction. This complex strategy of host-parasite relationship is much better exemplified by two helminth parasites: the trematode Schistosoma mansoni and the cestode Taenia crassiceps that respond to adrenal steroids and sexual steroids, respectively. Understanding how the host endocrine system can under certain circumstances favor the establishment of a parasitic infection opens interesting perspectives into the host-parasite relationship field.
Escobedo
Galileo
G
Departamento de Inmunología, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, México, México.
López-Griego
Lorena
L
Morales-Montor
Jorge
J
D000818:Animals; D005075:Biological Evolution; D003687:Dehydroepiandrosterone / Q000502:physiology; D005260:Female; D012739:Gonadal Steroid Hormones / Q000502:physiology; D006373:Helminthiasis / Q000276:immunology / Q000503:physiopathology*; D006374:Helminthiasis, Animal / Q000276:immunology / Q000503:physiopathology; D006376:Helminths / Q000502:physiology*; D006790:Host-Parasite Interactions / Q000276:immunology / Q000502:physiology*; D006801:Humans; D006854:Hydrocortisone / Q000502:physiology; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology; D008297:Male; D008322:Mammals / Q000469:parasitology / Q000502:physiology; D018448:Models, Immunological; D008959:Models, Neurological; D015213:Neuroimmunomodulation / Q000502:physiology*; D010913:Pituitary-Adrenal System / Q000503:physiopathology; D012098:Reproduction; D012555:Schistosomiasis mansoni / Q000276:immunology / Q000503:physiopathology; D012726:Sexual Behavior, Animal / Q000502:physiology; D013622:Taeniasis / Q000276:immunology / Q000503:physiopathology
D012739:Gonadal Steroid Hormones; D003687:Dehydroepiandrosterone; D006854:Hydrocortisone