Costa, T. R. et al. Secretion systems in Gram-negative bacteria: structural and mechanistic insights. Nat. Rev. Microbiol. 13, 343–359 (2015).
Mondino, S. et al. Legionnaires’ disease: state of the art knowledge of pathogenesis mechanisms of Legionella. Annu Rev Pathol 15, 439–466 (2020).
Green, E. R. & Mecsas, J. Bacterial secretion systems: an overview. Microbiol. Spectr. https://doi.org/10.1128/microbiolspec.VMBF-0012-2015 (2016).
Venter, J. C., Glass, J. I., Hutchison, C. A. 3rd & Vashee, S. Synthetic chromosomes, genomes, viruses, and cells. Cell 185, 2708–2724 (2022).
Martinez-Garcia, E. & de Lorenzo, V. The quest for the minimal bacterial genome. Curr. Opin. Biotechnol. 42, 216–224 (2016).
Sung, B. H., Choe, D., Kim, S. C. & Cho, B. K. Construction of a minimal genome as a chassis for synthetic biology. Essays Biochem 60, 337–346 (2016).
O’Connor, T. J., Adepoju, Y., Boyd, D. & Isberg, R. R. Minimization of the Legionella pneumophila genome reveals chromosomal regions involved in host range expansion. Proc. Natl Acad. Sci. USA 108, 14733–14740 (2011).
Ruano-Gallego, D. et al. Type III secretion system effectors form robust and flexible intracellular virulence networks. Science https://doi.org/10.1126/science.abc9531 (2021).
Chen, D. et al. Systematic reconstruction of an effector-gene network reveals determinants of Salmonella cellular and tissue tropism. Cell Host Microbe 29, 1531–1544 e1539 (2021).
Jennings, E., Thurston, T. L. M. & Holden, D. W. Salmonella SPI-2 type III secretion system effectors: molecular mechanisms and physiological consequences. Cell Host Microbe 22, 217–231 (2017).
Pillay, T. D. et al. Speaking the host language: how Salmonella effector proteins manipulate the host. Microbiology https://doi.org/10.1099/mic.0.001342 (2023).
Nuccio, S. P. & Baumler, A. J. Comparative analysis of Salmonella genomes identifies a metabolic network for escalating growth in the inflamed gut. mBio 5, e00929–00914 (2014).
Lesnick, M. L., Reiner, N. E., Fierer, J. & Guiney, D. G. The Salmonella spvB virulence gene encodes an enzyme that ADP-ribosylates actin and destabilizes the cytoskeleton of eukaryotic cells. Mol. Microbiol. 39, 1464–1470 (2001).
Haneda, T. et al. Salmonella type III effector SpvC, a phosphothreonine lyase, contributes to reduction in inflammatory response during intestinal phase of infection. Cell Microbiol. 14, 485–499 (2012).
Grabe, G. J. et al. The Salmonella effector SpvD is a cysteine hydrolase with a serovar-specific polymorphism influencing catalytic activity, suppression of immune responses, and bacterial virulence. J. Biol. Chem. 291, 25853–25863 (2016).
Steele-Mortimer, O., Meresse, S., Gorvel, J. P., Toh, B. H. & Finlay, B. B. Biogenesis of Salmonella Typhimurium-containing vacuoles in epithelial cells involves interactions with the early endocytic pathway. Cell. Microbiol. 1, 33–49 (1999).
Buchmeier, N. A. & Heffron, F. Inhibition of macrophage phagosome–lysosome fusion by Salmonella Typhimurium. Infect. Immun. 59, 2232–2238 (1991).
Galan, J. E. & Curtiss, R. 3rd Cloning and molecular characterization of genes whose products allow Salmonella Typhimurium to penetrate tissue culture cells. Proc. Natl Acad. Sci. USA 86, 6383–6387 (1989).
Brown, N. F. et al. Salmonella Pathogenicity Island 2 is expressed prior to penetrating the intestine. PLoS Pathog. 1, e32 (2005).
Cirillo, D. M., Valdivia, R. H., Monack, D. M. & Falkow, S. Macrophage-dependent induction of the Salmonella Pathogenicity Island 2 type III secretion system and its role in intracellular survival. Mol. Microbiol. 30, 175–188 (1998).
Becht, E. et al. Dimensionality reduction for visualizing single-cell data using UMAP. Nat. Biotechnol. https://doi.org/10.1038/nbt.4314 (2018).
Levine, J. H. et al. Data-driven phenotypic dissection of AML reveals progenitor-like cells that correlate with prognosis. Cell 162, 184–197 (2015).
Geddes, K., Cruz, F. & Heffron, F. Analysis of cells targeted by Salmonella type III secretion in vivo. PLoS Pathog. 3, e196 (2007).
Helaine, S. et al. Internalization of Salmonella by macrophages induces formation of nonreplicating persisters. Science 343, 204–208 (2014).
Hickey, M. J. et al. L-selectin facilitates emigration and extravascular locomotion of leukocytes during acute inflammatory responses in vivo. J. Immunol. 165, 7164–7170 (2000).
Xu, H., Manivannan, A., Crane, I., Dawson, R. & Liversidge, J. Critical but divergent roles for CD62L and CD44 in directing blood monocyte trafficking in vivo during inflammation. Blood 112, 1166–1174 (2008).
Scharer, C. D. et al. Antibody-secreting cell destiny emerges during the initial stages of B-cell activation. Nat. Commun. 11, 3989 (2020).
Ito, Y., Nakahara, F., Kagoya, Y. & Kurokawa, M. CD62L expression level determines the cell fate of myeloid progenitors. Stem Cell Rep. 16, 2871–2886 (2021).
Rydstrom, A. & Wick, M. J. Monocyte and neutrophil recruitment during oral Salmonella infection is driven by MyD88-derived chemokines. Eur. J. Immunol. 39, 3019–3030 (2009).
Adachi, O. et al. Targeted disruption of the MyD88 gene results in loss of IL-1- and IL-18-mediated function. Immunity 9, 143–150 (1998).
Akira, S. & Takeda, K. Toll-like receptor signalling. Nat. Rev. Immunol. 4, 499–511 (2004).
Kofoed, E. M. & Vance, R. E. Innate immune recognition of bacterial ligands by NAIPs determines inflammasome specificity. Nature 477, 592–595 (2011).
Zhao, Y. et al. The NLRC4 inflammasome receptors for bacterial flagellin and type III secretion apparatus. Nature 477, 596–600 (2011).
Rauch, I. et al. NAIP proteins are required for cytosolic detection of specific bacterial ligands in vivo. J. Exp. Med. 213, 657–665 (2016).
Perkins, D. J. et al. Salmonella Typhimurium co-opts the host type I IFN system to restrict macrophage innate immune transcriptional responses selectively. J. Immunol. 195, 2461–2471 (2015).
Wilson, R. P. et al. STAT2 dependent type I interferon response promotes dysbiosis and luminal expansion of the enteric pathogen Salmonella Typhimurium. PLoS Pathog. 15, e1007745 (2019).
Mastroeni, P. & Sheppard, M. Salmonella infections in the mouse model: host resistance factors and in vivo dynamics of bacterial spread and distribution in the tissues. Microbes Infect. 6, 398–405 (2004).
Carter, P. B. & Collins, F. M. The route of enteric infection in normal mice. J. Exp. Med. 139, 1189–1203 (1974).
Jones, B. D., Ghori, N. & Falkow, S. Salmonella Typhimurium initiates murine infection by penetrating and destroying the specialized epithelial M cells of the Peyer’s patches. J. Exp. Med. 180, 15–23 (1994).
Dieye, Y., Ameiss, K., Mellata, M. & Curtiss, R. 3rd The Salmonella Pathogenicity Island (SPI) 1 contributes more than SPI2 to the colonization of the chicken by Salmonella enterica serovar Typhimurium. BMC Microbiol. 9, 3 (2009).
Kappeli, R., Kaiser, P., Stecher, B. & Hardt, W. D. Roles of spvB and spvC in S. Typhimurium colitis via the alternative pathway. Int. J. Med. Microbiol. 301, 117–124 (2011).
Salcedo, S. P., Noursadeghi, M., Cohen, J. & Holden, D. W. Intracellular replication of Salmonella Typhimurium strains in specific subsets of splenic macrophages in vivo. Cell Microbiol. 3, 587–597 (2001).
Dunlap, N. E., Benjamin, W. H. Jr., McCall, R. D. Jr., Tilden, A. B. & Briles, D. E. A ‘safe-site’ for Salmonella Typhimurium is within splenic cells during the early phase of infection in mice. Microb. Pathog. 10, 297–310 (1991).
Hoffman, D. et al. A non-classical monocyte-derived macrophage subset provides a splenic replication niche for intracellular Salmonella. Immunity 54, 2712–2723 e2716 (2021).
Rosche, K. L., Aljasham, A. T., Kipfer, J. N., Piatkowski, B. T. & Konjufca, V. Infection with Salmonella enterica serovar Typhimurium leads to increased proportions of F4/80+ red pulp macrophages and decreased proportions of B and T lymphocytes in the spleen. PLoS ONE 10, e0130092 (2015).
Rydstrom, A. & Wick, M. J. Monocyte recruitment, activation, and function in the gut-associated lymphoid tissue during oral Salmonella infection. J. Immunol. 178, 5789–5801 (2007).
Richter-Dahlfors, A., Buchan, A. M. & Finlay, B. B. Murine salmonellosis studied by confocal microscopy: Salmonella Typhimurium resides intracellularly inside macrophages and exerts a cytotoxic effect on phagocytes in vivo. J. Exp. Med. 186, 569–580 (1997).
van der Velden, A. W., Lindgren, S. W., Worley, M. J. & Heffron, F. Salmonella pathogenicity island 1-independent induction of apoptosis in infected macrophages by Salmonella enterica serotype Typhimurium. Infect. Immun. 68, 5702–5709 (2000).
Robinson, N. et al. Type I interferon induces necroptosis in macrophages during infection with Salmonella enterica serovar Typhimurium. Nat. Immunol. 13, 954–962 (2012).
Hiyoshi, H. et al. Virulence factors perforate the pathogen-containing vacuole to signal efferocytosis. Cell Host Microbe 30, 163–170 e166 (2022).
Libby, S. J., Lesnick, M., Hasegawa, P., Weidenhammer, E. & Guiney, D. G. The Salmonella virulence plasmid spv genes are required for cytopathology in human monocyte-derived macrophages. Cell Microbiol. 2, 49–58 (2000).
Hoiseth, S. K. & Stocker, B. A. Aromatic-dependent Salmonella Typhimurium are non-virulent and effective as live vaccines. Nature 291, 238–239 (1981).
Kovach, M. E. et al. Four new derivatives of the broad-host-range cloning vector pBBR1MCS, carrying different antibiotic-resistance cassettes. Gene 166, 175–176 (1995).
Rong, S. et al. Expression of SREBP-1c requires SREBP-2-mediated generation of a sterol ligand for LXR in livers of mice. eLife https://doi.org/10.7554/eLife.25015 (2017).
