ArticlePLoS pathogens2012
InlA promotes dissemination of Listeria monocytogenes to the mesenteric lymph nodes during food borne infection of mice.
Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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Who cites it
68 citing papers in PubMed, 89 citations in OpenAlex.
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- GPR35 mediates monocyte recruitment to the sites of Listeria monocytogenes infection.Cellular and molecular life sciences : CMLS · 2025Article
- A genome-wide screen in ex vivo gallbladders identifies Listeria monocytogenes factors required for virulence in vivo.PLoS pathogens · 2025Article
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- Breaking Barriers: A Protocol to Investigate Intestinal Pathogen Adhesion, Invasion, and Translocation Through In Vitro, In Vivo, and Imaging Technologies.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Lymph node stromal cells vary in susceptibility to infection but can support the intracellular growth of Listeria monocytogenes.Journal of leukocyte biology · 2024Article
- Infectious factors in myocarditis: a comprehensive review of common and rare pathogens.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2024Review
- Temporal and spatial dynamics ofProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Current methodologies available to evaluate the virulence potential amongFrontiers in microbiology · 2024Review
- Catabolite control protein C contributes to virulence and hydrogen peroxide-induced oxidative stress responses inFrontiers in microbiology · 2024Article
- Apolipoprotein E genotype affects innate susceptibility toInfection and immunity · 2023Article
- Fecal Fungal Microbiota (Mycobiome) Study as a Potential Tool for Precision Medicine in Inflammatory Bowel Disease.Gut and liver · 2023Review
- A genome-wide screen in macrophages identifies PTEN as required for myeloid restriction of Listeria monocytogenes infection.PLoS pathogens · 2023Article
- Egress of Listeria monocytogenes from Mesenteric Lymph Nodes Depends on Intracellular Replication and Cell-to-Cell Spread.Infection and immunity · 2023Article
- The accumulation of Vγ4 T cells with aging is associated with an increased adaptive Vγ4 T cell response after foodborne Listeria monocytogenes infection of mice.Immunity & ageing : I & A · 2022Article
- The use of foodborne infection to evaluate bacterial pathogenesis and host response.Methods in cell biology · 2022Article
- Role of FruR transcriptional regulator in virulence of Listeria monocytogenes and identification of its regulon.PloS one · 2022Article
8 more citing papers are in PubMed but not listed here.
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6 authors at 2 institutions in 1 country.
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Abstract
Intestinal Listeria monocytogenes infection is not efficient in mice and this has been attributed to a low affinity interaction between the bacterial surface protein InlA and E-cadherin on murine intestinal epithelial cells. Previous studies using either transgenic mice expressing human E-cadherin or mouse-adapted L. monocytogenes expressing a modified InlA protein (InlA(m)) with high affinity for murine E-cadherin showed increased efficiency of intragastric infection. However, the large inocula used in these studies disseminated to the spleen and liver rapidly, resulting in a lethal systemic infection that made it difficult to define the natural course of intestinal infection. We describe here a novel mouse model of oral listeriosis that closely mimics all phases of human disease: (1) ingestion of contaminated food, (2) a distinct period of time during which L. monocytogenes colonize only the intestines, (3) varying degrees of systemic spread in susceptible vs. resistant mice, and (4) late stage spread to the brain. Using this natural feeding model, we showed that the type of food, the time of day when feeding occurred, and mouse gender each affected susceptibility to L. monocytogenes infection. Co-infection studies using L. monocytogenes strains that expressed either a high affinity ligand for E-cadherin (InlA(m)), a low affinity ligand (wild type InlA from Lm EGDe), or no InlA (ΔinlA) showed that InlA was not required to establish intestinal infection in mice. However, expression of InlA(m) significantly increased bacterial persistence in the underlying lamina propria and greatly enhanced dissemination to the mesenteric lymph nodes. Thus, these studies revealed a previously uncharacterized role for InlA in facilitating systemic spread via the lymphatic system after invasion of the gut mucosa.
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