TABLE 1.
Salmonella and host responses discussed in this chapter with probable impact on host-to-host transmission of the pathogen
| Host and/or pathogen response | Pathogen functions or effectors involveda | S. enterica serovar(s) in which it has been investigated | Reference(s) |
|---|---|---|---|
| Selection of persister bacteria inside macrophages | toxin-antitoxin (TA) loci | Typhimurium | 19 |
| Selection of small-colony variants in persistent infections of fibroblasts | hemL, lpd, and aroD (inactivating mutations) | Typhimurium | 75 |
| Production of toxins by the pathogen to restrain growth | TA loci (suspected in host) and TacT toxin | Typhimurium | 19, 135 |
| Pathogen proliferation in cytosol of epithelial cells | SPI-1 (T1), YdgT, CorA, and RecA | Typhimurium | 20, 21, 141 |
| Attenuation of pathogen proliferation inside fibroblasts | PhoP-PhoQ, RpoS, SlyA, IgaA | Typhimurium | 65 |
| SPI-1-mediated invasiveness | SPI-1 (T1) and dedicated effectors (SopB, SopE, SopE2, SipA, SipB, and SptP) | Typhimurium, Typhi, Enteritidis, and many other serovars | 142 |
| SPI-1-independent invasion and pathogenicity in animal models | RcsK and PagN; other? | Typhimurium, Enteritidis, and Gallinarum | 29, 34, 143 |
| Modulation of intracellular proliferation rate due to the presence or absence of defined Rab GTPases (Rab29, Rab32) in the SCV | GtgE (a T1/T2 effector) | Typhimurium and Typhi (ectopic expression of GtgE) | 50, 51 |
| Sifs supporting intracellular bacterial growth | SifA, SseJ (T2 effectors), and PLEKHM1 (host protein) | Typhimurium and Typhi | 53, 56 |
| Selective autophagy of a subpopulation of intracellular bacteria triggered by a membranous aggresome | SPI-2 | Typhimurium | 57 |
| Inflammasome activation in intestinal epithelial cells | NAIP/NLRC4 and caspase-1 (host proteins) | Typhimurium | 63 |
| Uptake of distinct carbon sources (polysaccharides?) by intracellular bacteria in chronically infected hosts | KdgR (proposed enhanced activity of this regulator) | Typhimurium | 77 |
| Uptake of nutrients (e.g., amino acids) via the Sif tubular membranous extensions | SPI-2 effectors involved in Sif formation; dedicated pathogen transporters? | Typhimurium | 78 |
| Active proliferation in the host (acute infection) | SPI-2; ubiquinone synthesis | Typhimurium | 82 |
| Persistence in host tissues and organs | FabB (β-ketoacyl-ACP synthase I): synthesis of unsaturated fatty acids and cyclopropane | Typhimurium | 82 |
| Sequestration of substrate to host enzyme, generating toxic compounds | DalS (pathogen d-Ala transporter), DAO (host enzyme generating toxic compounds from d-Ala) | Typhimurium | 111 |
| Maintenance of integrity of SCV membrane; increased ubiquitination of cytosolic bacteria | TBK1 (host protein) | Typhimurium | 109, 110 |
| Modulation of the inflammatory status of the pathogen (M1/M2) by intracellular bacteria | Unknown (response associated to bacterial load) | Typhimurium | 115 |
| High proliferation in a low percentage of infected cells in gallbladder and intestinal epithelia | Unknown | Typhimurium | 60, 63 |
a
SPI-1, Salmonella-pathogenicity island.