ArticleInfection and immunity2010
The stress-induced virulence protein InlH controls interleukin-6 production during murine listeriosis.
Article in Infection and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 44 citations in OpenAlex.
- Transcriptome Sequencing Reveals Distinct Stress Response of Listeria monocytogenes 6179 During Logarithmic and Stationary Growth Phases.MicrobiologyOpen · 2025Article
- Listeriosis.Nature reviews. Disease primers · 2025Review
- Biofilm Formation, Motility, and Virulence ofMicroorganisms · 2024Article
- Article
- A bacterial virulence factor interacts with the splicing factor RBM5 and stimulates formation of nuclear RBM5 granules.Scientific reports · 2022Article
- Article
- Virulence gene repression promotesGut microbes · 2020Article
- Innate and Adaptive Immune Responses duringMicrobiology spectrum · 2019Article
- Listeria monocytogenes and the Inflammasome: From Cytosolic Bacteriolysis to Tumor Immunotherapy.Current topics in microbiology and immunology · 2016Review
- Article
- Genome comparison of Listeria monocytogenes serotype 4a strain HCC23 with selected lineage I and lineage II L. monocytogenes strains and other Listeria strains.Genomics data · 2014Article
- How Listeria monocytogenes organizes its surface for virulence.Frontiers in cellular and infection microbiology · 2014Review
- The bacterial pathogen Listeria monocytogenes and the interferon family: type I, type II and type III interferons.Frontiers in cellular and infection microbiology · 2014Review
- Remodeling of the Listeria monocytogenes cell wall inside eukaryotic cells.Communicative & integrative biology · 2012Article
- Illuminating the landscape of host-pathogen interactions with the bacterium Listeria monocytogenes.Proceedings of the National Academy of Sciences of the United States of America · 2011Review
- Transcytosis of Listeria monocytogenes across the intestinal barrier upon specific targeting of goblet cell accessible E-cadherin.The Journal of experimental medicine · 2011Article
- Association of ActA to peptidoglycan revealed by cell wall proteomics of intracellular Listeria monocytogenes.The Journal of biological chemistry · 2011Article
- Regulated shift from helical to polar localization of Listeria monocytogenes cell wall-anchored proteins.Journal of bacteriology · 2011Article
- OatA, a peptidoglycan O-acetyltransferase involved in Listeria monocytogenes immune escape, is critical for virulence.The Journal of infectious diseases · 2011Article
- Genome sequence of the nonpathogenic Listeria monocytogenes serovar 4a strain M7.Journal of bacteriology · 2011Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
The genome of the pathogenic bacterium Listeria monocytogenes contains a family of genes encoding proteins with a leucine-rich repeat domain. One of these genes, inlH, is a sigma(B)-dependent virulence gene of unknown function. Previously, inlH was proposed to be coexpressed with two adjacent internalin genes, inlG and inlE. Using tiling arrays, we showed that inlH expression is monocistronic and specifically induced in stationary phase as well as in the intestinal lumen of mice, independent of inlG and inlE expression. Consistent with inlH sigma(B)-dependent regulation, surface expression of the InlH protein is induced when bacteria are subjected to thermal, acidic, osmotic, or oxidative stress. Disruption of inlH increases the amount of the invasion protein InlA without changing inlA transcript level, suggesting that there is a link between inlH expression and inlA posttranscriptional regulation. However, in contrast to InlA, InlH does not contribute to bacterial invasion of cultured cells in vitro or of intestinal cells in vivo. Strikingly, the reduced virulence of inlH-deficient L. monocytogenes strains is accompanied by enhanced production of interleukin-6 (IL-6) in infected tissues during the systemic phase of murine listeriosis but not by enhanced production of any other inflammatory cytokine tested. Since InlH does not modulate IL-6 secretion in macrophages at least in vitro, it may play a role in other immune cells or contribute to a pathway that modulates survival or activation of IL-6-secreting cells. These results strongly suggest that InlH is a stress-induced surface protein that facilitates pathogen survival in tissues by tempering the inflammatory response.
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Registered trials
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