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Biology subjects

Szabo, E. K.

Publications and source records attributed to Szabo, E. K..

2 recordsLinked to original sources

Evidence of opportunistic blood feeding in the parasitic nematode Heligmosomoides bakeri

Haem, which binds iron and oxygen, is essential for parasitic nematode growth. Nematodes lack endogenous haem synthesis pathways and acquire haem from their environment or intracellular symbionts. Genes involved in haem degradation and detoxification have been identified in parasitic nematodes who are either specialised blood feeders (haematophages) or reside in the blood stream. Targeting these genes, so limiting parasite growth and promoting parasite death, provides a new therapeutic avenue against blood feeding parasitic nematodes. Heligmosomoides bakeri, a model intestinal parasitic nematode, has not been considered a blood feeder. Adults live in the intestinal lumen and graze on host tissue. However, the earlier larval stages enter the intestinal tissue, where they grow and moult multiple times, an oxygen demanding process. We have shown that, in vivo, likely through nematode-induced damage, many tissue-dwelling H. bakeri are in close vicinity of red blood cells. During this time, infection induces host anemia. Further, tissue-dwelling H. bakeri that have fed on blood have an increased expression of collagen genes compared to those parasites that had not fed on blood. In vitro, this translates to a growth advantage. Our findings suggest blood feeding is more widespread among nematodes than currently described. We argue that biochemical adaptations previously considered to be limited to blood-feeders are found in other nematodes. Moreover, H. bakeri can serve as a model for studying blood-feeding mechanisms and developing anthelminthic strategies to them.

zoology↗

Early Th2 cytokine production in Heligmosomoides polygyrus and Toxoplasma gondii co-infected mice is associated with reduced IFNγ production, increased parasite loads and increased mortality

Co-infections are a common reality but understanding how the immune system responds in this context is complex and can be unpredictable. Heligmosomoides bakeri (parasitic roundworm, previously Heligmosomoides polygyrus) and Toxoplasma gondii (protozoan parasite) are well studied organisms that stimulate a characteristic Th2 and Th1 response, respectively. Several studies have demonstrated reduced inflammatory cytokine responses in animals co-infected with such organisms. However, while general cytokine signatures have been examined, the impact of the different cytokine producing lymphocytes on parasite control/clearance is not fully understood. We investigated five different lymphocyte populations (NK, NKT, {gamma}{delta} T, CD4 + T and CD8+ T cells), five organs (small intestine, Peyers patches, mesenteric lymph nodes, spleen and liver), and 4 cytokines (IFN {gamma}, IL-4, IL-10 and IL-13) at two different time points (days 5 and 10 post T. gondii infection). We found that co-infected animals had significantly higher mortality than either single infection. This was accompanied by transient and local changes in parasite loads and cytokine profiles. Despite the early changes in lymphocyte and cytokine profiles, severe intestinal pathology in co-infected mice likely contributed to early mortality due to significant damage by both parasites in the small intestine. Our work demonstrates the importance of taking a broad view during infection research, studying multiple cell types, organs/tissues and time points to link and/or uncouple immunological from pathological findings. Our results provide insights into how co-infection with parasites stimulating different arms of the immune system can lead to drastic changes in infection dynamics.

immunology↗