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Sci Rep. 2018 Aug 1;8(1):11547. doi: 10.1038/s41598-018-30058-9.

Hookworm exposure decreases human papillomavirus uptake and cervical cancer cell migration through systemic regulation of epithelial-mesenchymal transition marker expression.

Author information

1
Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Cape Town, 7925, South Africa.
2
Institute of Microbiology and Infection, University of Birmingham, B15 2TT, Birmingham, UK.
3
Le Studium Institute for Advanced Studies Laboratory of Molecular and Experimental Immunology and Neurogenetics, CNRS-University of Orleans, Rue Dupanloup, 45000, Orléans, France.
4
Department of Human Biology, University of Cape Town, Cape Town, 7925, South Africa.
5
Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Cape Town, 7925, South Africa. smithk28@cardiff.ac.uk.
6
School of Medicine, Cardiff University, Cardiff, CF14 4XN, UK. smithk28@cardiff.ac.uk.

Abstract

Persistent infection with human papillomavirus (HPV) is responsible for nearly all new cervical cancer cases worldwide. In low- and middle-income countries (LMIC), infection with helminths has been linked to increased HPV prevalence. As the incidence of cervical cancer rises in helminth endemic regions, it is critical to understand the interaction between exposure to helminths and the progression of cervical cancer. Here we make use of several cervical cancer cell lines to demonstrate that exposure to antigens from the hookworm N. brasiliensis significantly reduces cervical cancer cell migration and global expression of vimentin and N-cadherin. Importantly, N. brasiliensis antigen significantly reduced expression of cell-surface vimentin, while decreasing HPV type 16 (HPV16) pseudovirion internalization. In vivo infection with N. brasiliensis significantly reduced vimentin expression within the female genital tract, confirming the relevance of these in vitro findings. Together, these findings demonstrate that infection with the hookworm-like parasite N. brasiliensis can systemically alter genital tract mesenchymal markers in a way that may impair cervical cancer cell progression. These findings reveal a possible late-stage treatment for reducing cervical cancer progression using helminth antigens.

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