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Host Phenotype (host + phenotype)
Selected AbstractsRecruitment of host progenitor cells in rat liver transplants,HEPATOLOGY, Issue 2 2009Zhaoli Sun Despite major histocompatibility complex incompatibility, liver transplants from Lewis rats to dark agouti (DA) rats survive indefinitely without immunosuppression, and the studies we report sought the mechanism(s) responsible for this. At 1 year, most of the liver reacted positively to host anti-DA antibody. When small (50%) grafts were transplanted, recruitment was more rapid because most of the organ assumed the host phenotype at 3 months. After transplantation, the Y chromosome was detected in the hepatocytes of XX to XY grafts by both in situ hybridization and polymerase chain reaction. Further, livers from transgenic Lewis rats carrying strong green fluorescent protein (GFP) markers lost the marker with time after transplantation to DA, GFP-negative hosts. Few liver cells contained the Y chromosome in syngeneic XX to XY liver grafts or when the hosts of Lewis XX to DA XY allografts were treated with cyclosporine A at 10 mg/kg/day. This dosage also impeded enlargement of the liver at 10 days. Using GFP-positive XX Lewis donors transplanted to GFP-negative XY DA hosts, we found little Y DNA in GFP-positive cells at 10 days. Host-derived OV-6,positive and c-kit,positive, albumin-positive cells were present at 3-10 days, but cells with the CD34 marker were less common and some clearly still had the donor phenotype at 10 days. Cells positive for chemokine cysteine-X-cysteine receptor-4 increased with time and were abundant 1 month after transplantation. We conclude: (1) extrahepatic cells can differentiate into liver tissues; (2) regenerative stimuli accelerate stem cell recruitment; (3) both regeneration and recruitment are impeded by cyclosporine A immunosuppression, and (4) donor GFP-positive cells contained little host Y chromosome after transplantation, suggesting that cell fusion was uncommon and, therefore, unlikely to be the mechanism leading to the changes in genotype and phenotype we observed. (HEPATOLOGY 2008.) [source] Erythrocyte Lewis (A+B,) host phenotype is a factor with familial clustering for increased risk of Helicobacter pylori -related non-cardiac gastric cancerJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 6 2006MING-JEN SHEU Abstract Background:, The purpose of the present study was to test whether host erythrocyte Lewis phenotypes correlated with the risk of gastric cancers. Because of the association of gastric cancer with familial clustering, cancer relatives were investigated as to whether they had unique distribution of Lewis phenotypes. Methods:, The study prospectively enrolled 74 Helicobacter pylori -positive gastric cancer patients and 100 H. pylori -positive duodenal ulcer patients to serve as non-cancer controls after panendoscopy. In addition, 433 family members from the 74 index cancer and 100 non-cancer control patients were enrolled. All enrolled cases were checked for their H. pylori status and erythrocyte Lewis phenotypes, defined as Lea,b,, Lea,b+, Lea+b,, and Lea+b+ subtypes by the anti-Lea and anti-Leb monoclonal antibodies. Results:, These H. pylori -infected patients with gastric cancer had a higher rate of Lea+b, phenotype and a lower rate of Lea,b+ phenotype than the non-cancer duodenal ulcer controls (20.3% vs 9%; 51.4% vs 72%, P < 0.05). Among these H. pylori -infected patients, the risk of the patients with Lea+b, phenotype having gastric cancer was 3.15-fold higher as compared with those with the Lea,b+ phenotype (P = 0.02, 95% confidence interval: 1.26,7.87). The offspring and cousins of the cancer patients had a higher rate of Lea+b, phenotype as compared to either that of the spouses of cancer index patients or to that of the family members of the non-cancer control (P < 0.05). Conclusion:, Lea+b, phenotype of the H. pylori -infected host could be a risk factor (with familial clustering) for gastric carcinogenesis. [source] Epigenetic effects of infection on the phenotype of host offspring: parasites reaching across host generationsOIKOS, Issue 3 2008Robert Poulin Parasite-induced changes in host phenotype are now well-documented from a wide range of taxa. There is a growing body of evidence indicating that parasites can also have trans-generational consequences, with infection of a host leading to changes in the phenotype of its offspring, though the latter are not parasitised. Several proximate mechanisms have been put forward to explain these ,maternal' effects, most involving hormonal or other physiological pathways, ultimately leading to offspring that are pre-adapted to the parasites they are most likely to encounter based on their mother's experience. Here, we propose that all these trans-generational effects on offspring phenotype must involve epigenetic phenomena. Epigenetics concerns the appearance and inheritance of seemingly new phenotypic traits without changes in the underlying DNA sequence. Since diet and other environmental factors experienced by a mother can affect gene expression in her offspring by turning genes ,on' or ,off' (for example, via DNA methylation), why couldn't parasites do it? Although epigenetic effects have not been explicitly invoked to account for trans-generational impacts of parasites on the phenotype of host offspring, the existing evidence is fully compatible with their involvement. We argue that epigenetic mechanisms must play a central role; we also discuss their evolutionary implications and suggest questions for future investigations in this new and exciting research direction. [source] Variation in stickleback head morphology associated with parasite infectionBIOLOGICAL JOURNAL OF THE LINNEAN SOCIETY, Issue 4 2009NIELS J. DINGEMANSE Parasites can affect host phenotypes, influencing their ecology and evolution. Host morphological changes occurring post-infection might result from pathological by-products of infection, or represent adaptations of hosts or parasites. We investigated the morphology of three-spined sticklebacks, Gasterosteus aculeatus, from a population naturally infected with Schistocephalus solidus, which grows to large sizes in their body cavity. We examined local effects of infection on trunk shape, which are imposed directly by the bulk of the growing parasite, and distant effects on head morphology. We show that trunk shape differed between infection classes, and was affected more severely in fish with heavier total parasite mass. We further show unexpected differences in head morphology. The heads of infected fish were reduced in size and differently shaped to those of non-infected fish, with infected fish having deeper heads. Importantly, both head size and shape were also affected more severely in fish with heavier total parasite mass. This latter result suggests that differences in morphology are caused by post-infection changes. Such changes may be incidental, evolutionarily neutral ,side effects' of infection. However, because head morphology affects foraging ecology, such changes are likely to have fitness consequences for hosts, and may constitute adaptations, either of hosts or of parasites. We discuss our finding in the context of the evolution of phenotypic plasticity, and suggest testable hypotheses examining the proximate mechanisms underlying these morphological effects and their potential evolutionary basis. © 2009 The Linnean Society of London, Biological Journal of the Linnean Society, 2009, 96, 759,768. [source] | |||||||||||||