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Imaging InlC Secretion to Investigate Cellular Infection by the Bacterial Pathogen Listeria monocytogenes
Published on: September 19, 2013
Transcriptome responses of intestinal epithelial cells induced by membrane vesicles of Listeria
Raman Karthikeyan1, Pratapa Gayathri2, Subbiah Ramasamy3
1Department of Genetics, School of Biological Sciences, Madurai Kamaraj University, Madurai, 625021, Tamil Nadu, India.
Abstract:
Membrane vesicles (MVs) serve as an essential virulence factor in several pathogenic bacteria. The release of MVs by Listeria monocytogenes is only recently recognized; still, the enigmatic role of MVs in pathogenesis is yet to be established. We report the transcriptome response of Caco-2 cells upon exposure to MVs and the L. monocytogenes that leads to observe the up-regulation of autophagy-related genes in the early phase of exposure to MVs. Transcription of inflammatory cytokines is to the peak at the fourth hour of exposure. An array of differentially expressed genes was associated with actin cytoskeleton rearrangement, autophagy, cell cycle arrest, and induction of oxidative stress. At a later time point, transcriptional programs are generated upon interaction with MVs to evade innate immune signals, by modulating the expression of anti-inflammatory genes. KEGG pathway analysis is palpably confirming that MVs appear principally responsible for the induction of immune signaling pathways. Besides, MVs induced the expression of cell cycle regulatory genes, likely responsible for the ability to prolong host cell survival, thus protecting the replicative niche for L. monocytogenes. Notably, we identified several non-coding RNAs (ncRNAs), possibly involved in the regulation of early manipulation of the host gene expression, essential for the persistence of L. monocytogenes.
Insights
Membrane vesicles (MVs) from Listeria monocytogenes trigger host cell responses, including autophagy and inflammation. These MVs manipulate host gene expression to promote bacterial persistence and evade immune detection.
Area of Science:
- Microbiology
- Molecular Biology
- Immunology
Background:
- Membrane vesicles (MVs) are emerging virulence factors in pathogenic bacteria.
- The role of MVs from Listeria monocytogenes in pathogenesis is not well understood.
Purpose of the Study:
- To investigate the host cell transcriptome response to MVs from Listeria monocytogenes.
- To elucidate the mechanisms by which MVs contribute to Listeria monocytogenes pathogenesis.
Main Methods:
- Transcriptome analysis (RNA sequencing) of Caco-2 cells exposed to MVs and Listeria monocytogenes.
- KEGG pathway analysis to identify affected biological pathways.
- Identification of differentially expressed genes and non-coding RNAs (ncRNAs).
Main Results:
- Early exposure to MVs up-regulated autophagy-related genes.
- Inflammatory cytokine transcription peaked at 4 hours post-exposure.
- MVs induced genes involved in actin cytoskeleton rearrangement, cell cycle arrest, oxidative stress, and immune evasion.
- KEGG analysis confirmed MVs induce immune signaling pathways.
- MVs modulated anti-inflammatory gene expression for immune evasion.
- MVs induced cell cycle regulatory genes, potentially prolonging host cell survival.
- Several ncRNAs were identified, possibly regulating early host gene expression manipulation.
Conclusions:
- Listeria monocytogenes MVs significantly alter host cell gene expression, influencing autophagy, inflammation, and cell cycle.
- MVs play a crucial role in Listeria monocytogenes pathogenesis by modulating host responses and promoting bacterial persistence.
- ncRNAs within MVs may be key regulators of host-pathogen interactions.
