title: Transmissible Plasmid Containing Salmonella enterica Heidelberg Isolates Modulate Cytokine Production During Early Stage of Interaction with Intestinal Epithelial Cells.
abstract: The variation in cytokine production during bacterial invasion of human intestinal epithelial cells (IECs) is a contributing factor for progression of the infection. A few Salmonella enterica Heidelberg strains isolated from poultry products harbor transmissible plasmids (TPs), including those that encode a type-IV secretion system. Earlier, we showed that these TPs are responsible for increased virulence during infection. This study examines the potential role of these TPs in cytokine production in IECs. This study showed that S. Heidelberg strains containing TPs (we refer as virulent strains) caused decreased interleukin (IL)-10 production in IECs after 1 h infection. The virulent strains induced a high level of tumor necrosis factor-α production under identical conditions. The virulent strains of S. Heidelberg also altered the production of IL-2, IL-17, and granulocyte macrophage colony-stimulating factor compared to an avirulent strain. As a part of infection, bacteria cross the epithelial barrier and encounter intestinal macrophages. Hence, we examined the cytotoxic mechanism of strains of S. Heidelberg in macrophages. Scanning electron microscopy showed cell necrosis occurs during the early stage of infection. In conclusion, virulent S. Heidelberg strains were able to modify the host cytokine profile during the early stages of infection and also caused necrosis in macrophages.
authors.affiliation: Division of Microbiology, National Center for Toxicological Research , U.S. Food and Drug Administration, Jefferson, Arkansas.
authors.forename: Kuppan
authors.initials: K
authors.lastname: Gokulan
authors.affiliation: Division of Microbiology, National Center for Toxicological Research , U.S. Food and Drug Administration, Jefferson, Arkansas.
authors.forename: Sangeeta
authors.initials: S
authors.lastname: Khare
authors.affiliation: Division of Microbiology, National Center for Toxicological Research , U.S. Food and Drug Administration, Jefferson, Arkansas.
authors.forename: Katherine
authors.initials: K
authors.lastname: Williams
authors.affiliation: Division of Microbiology, National Center for Toxicological Research , U.S. Food and Drug Administration, Jefferson, Arkansas.
authors.forename: Steven L
authors.initials: SL
authors.lastname: Foley
mesh_terms: D000818:Animals; D002460:Cell Line; D002645:Chickens; D004847:Epithelial Cells / Q000276:immunology* / Q000382:microbiology; D015870:Gene Expression; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000096:biosynthesis / Q000276:immunology; D054884:Host-Pathogen Interactions; D006801:Humans; D016753:Interleukin-10 / Q000096:biosynthesis / Q000276:immunology; D020381:Interleukin-17 / Q000096:biosynthesis / Q000276:immunology; D007413:Intestinal Mucosa / Q000276:immunology / Q000382:microbiology; D008264:Macrophages / Q000276:immunology* / Q000382:microbiology / Q000648:ultrastructure; D051379:Mice; D010957:Plasmids / Q000378:metabolism*; D019779:Salmonella enterica / Q000235:genetics / Q000302:isolation & purification / Q000472:pathogenicity / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000276:immunology
chemical_list: C508609:IL10 protein, human; D020381:Interleukin-17; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D016178:Granulocyte-Macrophage Colony-Stimulating Factor