Cooperation of<i>Salmonella</i>pathogenicity islands 1 and 4 is required to breach epithelial barriers

Gerlach, Roman G.; Cláudio, Nuno; Rohde, Manfred; Jäckel, Daniela; Wagner, Carolin; Hensel, Michael

doi:10.1111/j.1462-5822.2008.01218.x

Cited by 126 publications

(146 citation statements)

References 34 publications

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“…Although type III secretion system-mediated invasion of epithelial cells by S. enterica is inhibited by high c-di-GMP levels (333), some DGCs were found to stimulate invasion (311). This may be another case where c-di-GMP-inhibited type III secretion is countered by c-di-GMPstimulated adhesion via type IV pili, which are required for invasion (348)(349)(350).…”

Section: Cyclic Di-gmp and Virulencementioning

confidence: 99%

Cyclic di-GMP: the First 25 Years of a Universal Bacterial Second Messenger

Römling

Galperin

Gomelsky

2013

Microbiol Mol Biol Rev

1,444

1,698

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SUMMARY Twenty-five years have passed since the discovery of cyclic dimeric (3′→5′) GMP (cyclic di-GMP or c-di-GMP). From the relative obscurity of an allosteric activator of a bacterial cellulose synthase, c-di-GMP has emerged as one of the most common and important bacterial second messengers. Cyclic di-GMP has been shown to regulate biofilm formation, motility, virulence, the cell cycle, differentiation, and other processes. Most c-di-GMP-dependent signaling pathways control the ability of bacteria to interact with abiotic surfaces or with other bacterial and eukaryotic cells. Cyclic di-GMP plays key roles in lifestyle changes of many bacteria, including transition from the motile to the sessile state, which aids in the establishment of multicellular biofilm communities, and from the virulent state in acute infections to the less virulent but more resilient state characteristic of chronic infectious diseases. From a practical standpoint, modulating c-di-GMP signaling pathways in bacteria could represent a new way of controlling formation and dispersal of biofilms in medical and industrial settings. Cyclic di-GMP participates in interkingdom signaling. It is recognized by mammalian immune systems as a uniquely bacterial molecule and therefore is considered a promising vaccine adjuvant. The purpose of this review is not to overview the whole body of data in the burgeoning field of c-di-GMP-dependent signaling. Instead, we provide a historic perspective on the development of the field, emphasize common trends, and illustrate them with the best available examples. We also identify unresolved questions and highlight new directions in c-di-GMP research that will give us a deeper understanding of this truly universal bacterial second messenger.

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Section: Cyclic Di-gmp and Virulencementioning

confidence: 99%

Cyclic di-GMP: the First 25 Years of a Universal Bacterial Second Messenger

Römling

Galperin

Gomelsky

2013

Microbiol Mol Biol Rev

1,444

1,698

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“…For example, MisL contributes to Salmonella colonization in mice, chickens, and pigs but does not play a significant role in calves (42,43), while ShdA influenced S. Typhimurium persistence in mice but not in pigs (78,79). SPI-4 has been reported to mediate adherence to and invasion of bovine ileal mucosa, possibly in combination with the SPI-1 T3SS, but not in chickens and pigs (41,43,80).…”

Section: Salmonella Pathogenicity Islandsmentioning

confidence: 99%

Salmonella Pathogenicity and Host Adaptation in Chicken-Associated Serovars

Foley

Johnson

Ricke

et al. 2013

Microbiol Mol Biol Rev

247

218

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SUMMARY Enteric pathogens such as Salmonella enterica cause significant morbidity and mortality. S. enterica serovars are a diverse group of pathogens that have evolved to survive in a wide range of environments and across multiple hosts. S. enterica serovars such as S . Typhi, S . Dublin, and S . Gallinarum have a restricted host range, in which they are typically associated with one or a few host species, while S . Enteritidis and S . Typhimurium have broad host ranges. This review examines how S. enterica has evolved through adaptation to different host environments, especially as related to the chicken host, and continues to be an important human pathogen. Several factors impact host range, and these include the acquisition of genes via horizontal gene transfer with plasmids, transposons, and phages, which can potentially expand host range, and the loss of genes or their function, which would reduce the range of hosts that the organism can infect. S . Gallinarum, with a limited host range, has a large number of pseudogenes in its genome compared to broader-host-range serovars. S. enterica serovars such as S . Kentucky and S . Heidelberg also often have plasmids that may help them colonize poultry more efficiently. The ability to colonize different hosts also involves interactions with the host's immune system and commensal organisms that are present. Thus, the factors that impact the ability of Salmonella to colonize a particular host species, such as chickens, are complex and multifactorial, involving the host, the pathogen, and extrinsic pressures. It is the interplay of these factors which leads to the differences in host ranges that we observe today.

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“…For example, multiple attenuating mutations were identified in SPI-4 in calves, but not chickens or pigs challenged with the same library (Morgan et al 2004;Carnell et al 2007). SPI-4 encodes a Type I protein secretion system that secretes a ca 595 kDa protein (SiiE; Morgan et al 2007) that mediates adherence (Gerlach et al 2007) and invasion of bovine ileal mucosa , possibly by working in concert with T3SS-1 (Gerlach et al 2008). It is unlikely that SPI-4 acts in a fully bovine-specific manner, as SPI-4 mutants exhibited reduced virulence following oral inoculation of mice (Morgan et al 2004;Gerlach et al 2007).…”

Section: Molecular Basis Of Intestinal Colonization Of Food-producingmentioning

confidence: 99%

Molecular insights into farm animal and zoonoticSalmonellainfections

Stevens

Humphrey

Maskell

2009

Phil. Trans. R. Soc. B

142

102

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Salmonella enterica is a facultative intracellular pathogen of worldwide importance. Infections may present in a variety of ways, from asymptomatic colonization to inflammatory diarrhoea or typhoid fever depending on serovar-and host-specific factors. Human diarrhoeal infections are frequently acquired via the food chain and farm environment by virtue of the ability of selected non-typhoidal serovars to colonize the intestines of food-producing animals and contaminate the avian reproductive tract and egg. Colonization of reservoir hosts often occurs in the absence of clinical symptoms; however, some S. enterica serovars threaten animal health owing to their ability to cause acute enteritis or translocate from the intestines to other organs causing fever, septicaemia and abortion. Despite the availability of complete genome sequences of isolates representing several serovars, the molecular mechanisms underlying Salmonella colonization, pathogenesis and transmission in reservoir hosts remain ill-defined. Here we review current knowledge of the bacterial factors influencing colonization of food-producing animals by Salmonella and the basis of host range, differential virulence and zoonotic potential.

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Cooperation ofSalmonellapathogenicity islands 1 and 4 is required to breach epithelial barriers

Cited by 126 publications

References 34 publications

Cyclic di-GMP: the First 25 Years of a Universal Bacterial Second Messenger

Cyclic di-GMP: the First 25 Years of a Universal Bacterial Second Messenger

Salmonella Pathogenicity and Host Adaptation in Chicken-Associated Serovars

Molecular insights into farm animal and zoonoticSalmonellainfections

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