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Invasiveness of Shigella flexneri in poliovirus infected HT-29 cells
L Seganti1, M P Conte, C Longhi
1Istituto Pasteur-Fondazione Cenci Bolognetti, Università La Sapienza, Roma, Italy.
Abstract:
In this paper we report the effect in HT-29 cells of mixed infections with poliovirus type 1 and Shigella flexneri serotype 5 strain M90T and derivative strains differing in adhesive as well as invasive properties. HT-29 epithelial intestinal cells derived from a human colon adenocarcinoma are a good model for coinfection studies because they are susceptible both to poliovirus replication and to S. flexneri invasion. The results show that 48 h after infection by poliovirus the invasiveness of wild-type S. flexneri M90T and of its adherent and invasive derivative M90T (pIL22) is increased. However, the alterations produced in HT-29 cells at the later stage of poliovirus infection are not sufficient to promote the internalization of simply non invasive, or non invasive but adherent, isogenic derivative bacterial strains.
Insights
Poliovirus infection enhances Shigella flexneri invasion in HT-29 cells. However, poliovirus-induced cell changes do not enable non-invasive bacterial strains to enter these intestinal cells.
Area of Science:
- Microbiology
- Virology
- Cell Biology
Background:
- HT-29 cells, derived from human colon adenocarcinoma, are susceptible to poliovirus replication and Shigella flexneri invasion.
- Coinfection studies require cell models that can be infected by both pathogens.
Purpose of the Study:
- To investigate the effects of poliovirus type 1 infection on the invasiveness of Shigella flexneri serotype 5 in HT-29 cells.
- To determine if poliovirus-induced alterations in HT-29 cells can facilitate the invasion of non-invasive or adherent-non-invasive bacterial strains.
Main Methods:
- HT-29 cells were coinfected with poliovirus type 1 and wild-type Shigella flexneri M90T or its derivative strains.
- Bacterial invasiveness was assessed 48 hours post-infection.
Main Results:
- Poliovirus infection significantly increased the invasiveness of wild-type S. flexneri M90T and its adherent-invasive derivative M90T (pIL22).
- Late-stage poliovirus infection did not promote the internalization of isogenic S. flexneri derivatives that were non-invasive or only adherent.
Conclusions:
- Poliovirus infection modulates the intestinal cell environment, enhancing the invasiveness of certain Shigella flexneri strains.
- The cellular alterations induced by poliovirus are insufficient to overcome the intrinsic non-invasive nature of specific bacterial mutants.