PubMed · 13087715
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G HERTZBERG. 1953-06-19. [Pulmonary amebiasis].. https://pubmed.ncbi.nlm.nih.gov/13087715/
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Neoparamoeba spp. are amphizoic amoebae with the capacity to colonize the gills of some marine fish, causing AGD. Here, the gill tissue transcriptome response of Atlantic salmon (Salmo salar L.) to AGD is described. Tanks housing Atlantic salmon were inoculated with Neoparamoeba spp. and fish sampled at time points up to 8 days postinoculation (pi.). Gill tissues were taken from AGD-affected fish, and a DNA microarray was used to compare global gene expression against tissues from AGD-unaffected fish. A total of 206 genes, representing 190 unique transcripts, were reproducibly identified as up- or downregulated in response to Neoparamoeba spp. infection. Informative transcripts having GO biological process identifiers were grouped according to function. Although a number of genes were placed into each category, no distinct patterns were observed. One Atlantic salmon cDNA that was upregulated in infected gill relative to noninfected gill at 114 and 189 h pi. showed significant identity with the Xenopus, mouse, and human anterior gradient-2 (AG-2) homologs. Two Atlantic salmon AG-2 mRNA transcripts, designated asAG-2/1 and asAG-2/2, were cloned, sequenced, and shown to be predominantly expressed in the gill, intestine, and brain of a healthy fish. In AGD-affected fish, differential asAG-2 expression was confirmed in samples used for microarray analyses as well as in AGD-affected gill tissue taken from fish in an independent experiment. The asAG-2 upregulation was restricted to AGD lesions relative to unaffected tissue from the same gill arch, while p53 tumor suppressor protein mRNA was concurrently downregulated in AGD lesions. Differential expression of p53-regulated transcripts, proliferating cell nuclear antigen and growth arrest and DNA damage-inducible gene-45beta (GADD45beta) in AGD lesions, suggests a role for p53 in AGD pathogenesis. Thus AGD may represent a novel model for comparative analysis of p53 and p53-regulated pathways.
The differentiation of the two Entamoeba species E. histolytica and E. dispar through molecular characterization in the last decade of the twentieth century led to the need to re-evaluate the epidemiology of amebiasis in terms of prevalence and morbidity of the infection in the world's population, particularly in those geographic regions with high endemic rates.
The use of in vivo animal models in amebiasis has contributed significantly to the knowledge of this common human parasitic disease. Although there is no animal model that mimics the whole cycle of the human disease, the use of different susceptible and resistant laboratory animals and the availability for many years of techniques for the axenic culture of trophozoites of Entamoeba histolytica have allowed a better understanding of the parasite and the host-parasite relationship. The recent introduction of frontier methodologies in biology has increased our comprehension of this parasite. New information on the cellular and molecular biology and genetics of this organism has been extensively reported, and much of this has clearly required the more frequent use of animal models to verify specific facts. Based on experimental animals characterized previously, the introduction of new animal models with genetic or surgical modifications, especially in mice, has allowed a more adequate analysis of the mechanisms of pathogenesis. Multiple factors have been considered in the promotion of the invasiveness and virulence of E. histolytica. Additionally, the immunological and physiological responses of the host, depending on the environmental conditions, lead to the establishment or the rejection of the parasite. The role of inflammatory reaction to amebic infection constitutes one of the controversies that has been studied by several authors. In susceptible animals (hamsters and gerbils), inflammatory cell damage seems to be related to target cell lysis, while in resistant animals (mice), inflammatory cells appear to protect the host by lysing the parasite. Presently, the involvement of various substances in the development of lesions including lectins, proteases, amebapores, promoters of apoptosis, cytokines, nitric oxide, etc., is being examined using different in vivo models.