Iris Bruchhaus

...is a biologist specialising in parasitology. She completed her biology studies at the University of Hamburg (UHH) and then did her doctorate at the Bernhard Nocht Institute for Tropical Medicine (BNITM) in the Department of Molecular Parasitology under the supervision of Egbert Tannich. She then continued her work in Tannich's laboratory, supported by a DFG habilitation scholarship. In 2000, she habilitated at UHH and was appointed extraordinary professor in 2007. From 2000-2017, she was laboratory head in the Department of Molecular Parasitology and since 2018, she has headed the "Biology of Host-Parasite Interactions" group at BNITM.

since 2018 head of Biology of Host-Parasite Interactions group, BNITM

2000-2017 lab head in Department of Molecular Parasitology, BNITM

2007 appoointed extraordinary professor

2000 Habilitation at University of Hamburg

We are mainly interested in the interaction between parasites and their hosts. The parasites Entamoebae histolytica (causative agent of amoebiasis) and Plasmodium falciparum (causative agent of malaria) are the focus of our research.

The pathogen E. histolytica can live asymptomatically in the human gut, or it can disrupt the intestinal barrier and induce life-threatening abscesses in different organs, most often in the liver. The molecular framework that enables this invasive, highly pathogenic phenotype is still not well understood. To identify factors correlated with gut invasion and liver destruction, we have a unique tool available: E. histolytica clones that differ drastically in their virulence but have an almost identical genetic background. Using these clones, different silencing and overexpression methods, comparative proteome and transcriptome studies, and human and mouse 2D organoid models, we study the invasion process and the interaction between amoebae and host.

A major virulence determinant of P. falciparum is attributed to the ability of P. falciparum-infected erythrocytes (IEs) to evade the immune system and adhere in small blood vessels of vital organs, most commonly the small intestine, heart, lung, and brain within the human host. This cytoadhesion of IEs to endothelial cell receptors (ECRs) is the major reason for the most severe pathological phenotypes observed in malaria, which include blood flow obstruction, induction of inflammatory immune responses, endothelial dysfunction, tissue damage, and ultimately organ failure.  

The interaction of IEs with ECRs is mainly mediated by members of the PfEMP1 family.  We are particularly interested in characterising the interaction between the different PfEMP1s and ECRs and their relevance to pathology: i) Identification of PfEMP1 domains mediating cytoadhesion to different ECRs; ii) Characterisation of receptor-ligand phenotypes using a laminar flow system and atomic force microscopy; iii) Identification of novel endothelial receptors involved in cytoadhesion of infected erythrocytes; iv) Response of human primary endothelial cells due to interaction with IEs.

This study is Project 3 of the SPP 2332 PoP.