Regression models to assess the risk factors of canine gastrointestinal parasitism.

Gastrointestinal parasites, protozoa and helminths, remain a common important finding in dogs presented to veterinary medical practices. Moreover, dogs may play an active role in the transmission of enteric parasites to humans, given their cohabitation, making canine gastrointestinal parasitism an issue of major concern for public health. To get an overview of the current state of canine gastrointestinal parasites' prevalence in Greece, a total of 1036 faecal samples were collected from dogs either presented in veterinary clinics or in animal shelters. Samples were examined by a combined sedimentation-flotation technique. Possible risk factors (age, ownership status, co-existence with other animals, coinfection with other parasites) were assessed using binary regression models for each one of the most prevalent parasites. The overall gastrointestinal parasite prevalence in dogs' faecal samples was 39%. A total of 11 intestinal parasitic species were detected and up to five different parasites were isolated in the same faecal sample. Toxocara canis was the most prevalent parasite in the studied population, followed by Isospora spp., Giardia spp., Uncinaria spp., Trichuris vulpis, Ancylostoma spp., Toxascaris leonina, and Dipylidium caninum. Additionally, other genera (Taenia, Capillaria and Angiostrongylus) were also detected in very low percentages. Young, stray, living without other dogs, coinfected with T. vulpis or T. canis and free of Isospora spp. dogs were more likely to be infected by Giardia spp. Likewise, young, stray, coinfected with T. vulpis or T. canis but free of Giardia spp. dogs were more likely to be infected by Isospora spp. T. canis infections were more common in dogs coinfected with Isospora spp., Giardia spp., D. caninum, Τaenia spp., T. vulpis and T. leonina Finally, T. vulpis more often infected older dogs and dogs coinfected with Isospora spp., Giardia spp. and T. canis Consequently, the prevalence of parasitized dogs was high and the diversity of parasites found was notable, which calls for a greater awareness among veterinarians and pet owners. The proposed prediction models should be taken under consideration in diagnostic approach of clinical cases, as well as in planning sustainable antiparasitic strategies.

Licensing of DNA replication, cancer, pluripotency and differentiation: an interlinked world?

Recent findings provide evidence for a functional interplay between DNA replication and the seemingly distinct areas of cancer, development and pluripotency. Protein complexes participating in DNA replication origin licensing are now known to have roles in development, while their deregulation can lead to cancer. Moreover, transcription factors implicated in the maintenance of or reversal to the pluripotent state have links to the pre-replicative machinery. Several studies have shown that overexpression of these factors is associated to cancer.

Modulation of NF-kappaΒ signalling pathways by parasites.

NF-kappaB is implicated in lymphocyte development, maturation, proliferation and survival. This inducible transcription factor is widely expressed by virtually all cell types. In mammals, the genes rela, relb, crel, nfkappaΒ1, and nfkappaB encode the five NF-kB protein family members RelA (p65), RelB, c-Rel, p50, and p52, respectively, which form homo- and heterodimeric DNA-binding complexes capable of regulating target gene transcription of specific biological responses differentially. NF-kappaB regulates the expression of a wide variety of genes that play critical roles in innate and adaptive immune responses, is strongly linked to the inhibition of apoptosis, and contributes to tumor growth, metastasis, and chemoresistance. Parasites have targeted several parts of the NF-kappaB pathway, allowing them to interfere with the transcription of immune response genes. The biology of different parasites is critical in influencing the patterns and kinetics of NF-kappaB activity and thereby the development of subsequent immune responses.

Microarray analysis of NF-kappaB signaling pathways in PBMC of mice infected by Trichinella spiralis.

The NF-kappaΒ pathway gene expression profiles were compared between 10, 20 and 39 days after Trichinella spiralis experimental infection in BALB/c mice. Out of 128 genes, 19 (14.8%) genes were present in non-infected and post-infected mice. The expression of 7 (36.8%) genes was downregulated 10 and 20 days post-infection while 3 (15.8%) genes were upregulated 39 days post-infection. The present study lists the candidate genes of the NF-kappaB signaling pathway that were commonly and differentially expressed between the specific points of T. spiralis infection, thus suggesting that these genes need to be further investigated to reveal the mechanism of the T. spiralis modulation of the NF-kappaB signaling pathways.

Involvement of NK cells against tumors and parasites.

Host resistance against pathogens depends on a complex interplay of innate and adaptive immune mechanisms. Acting as an early line of defence, the immune system includes activation of neutrophils, tissue macrophages, monocytes, dendritic cells, eosinophils and natural killer (NK) cells. NK cells are lymphoid cells that can be activated without previous stimulation and are therefore like macrophages in the first line of defence against tumor cells and a diverse range of pathogens. NK cells mediate significant activity and produce high levels of proinflammatory cytokines in response to infection. Their cytotoxicity production is induced principally by monocyte-, macrophage- and dendritic cell-derived cytokines, but their activation is also believed to be cytokine-mediated. Recognition of infection by NK cells is accomplished by numerous activating and inhibitory receptors on the NK cells' surface that selectively trigger the cytolytic activity in a major histocompability complex-independent manner. NK cells have trypanocidal activity of fibroblast cells and mediate direct destruction of extracellular epimastigote and trypomastigote forms of T. cruzi and T. lewisi in vitro; moreover, they kill plasmodia-infected erythrocytes directly through cell-cell interaction. This review provides a more detailed analysis of how NK cells recognize and respond to parasites and how they mediate cytotoxicity against tumor cells. Also the unique role of NK cells in innate immunity to infection and the relationship between parasites and carcinogenesis are discussed.