The current <i>Salmonella</i>‐host interactome

Schleker, Sylvia; Sun, Jingjing; Balachandran, Raghavan; Srnec, Matthew N.; Müller, Nicole; Koepfinger, Mary; Murthy, Leelavati R.; Zhao, Zhongming; Klein‐Seetharaman, Judith

doi:10.1002/prca.201100083

Cited by 57 publications

(67 citation statements)

References 116 publications

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“…The T3SSs are multiprotein complexes composed of structural and regulatory elements that transfer functional effectors from the bacterium into host cells, thereby facilitating invasion of and survival within host cells (48,49). The T3SSs play vital roles in the interaction of Salmonella with the host (238). Variations in the gene sequences encoding T3SS factors for both the SPI-1 and SPI-2 systems have been associated with differences in the abilities to invade different hosts.…”

Section: Examples Of Salmonella Host Range In Chicken-related Serovarsmentioning

confidence: 99%

Salmonella Pathogenicity and Host Adaptation in Chicken-Associated Serovars

Foley

Johnson

Ricke

et al. 2013

Microbiol Mol Biol Rev

261

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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Section: Examples Of Salmonella Host Range In Chicken-related Serovarsmentioning

confidence: 99%

Salmonella Pathogenicity and Host Adaptation in Chicken-Associated Serovars

Foley

Johnson

Ricke

et al. 2013

Microbiol Mol Biol Rev

261

218

View full text Add to dashboard Cite

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“…Defining the biochemical activities and cellular targets [150] of T3SS effectors are the initial steps to understand their function. As seen in Table 1, this information is missing for a significant number of known Salmonella effectors.…”

Section: Biochemical Activities and Host Targetsmentioning

confidence: 99%

Impact ofSalmonella entericaType III Secretion System Effectors on the Eukaryotic Host Cell

Ramos‐Morales

2012

ISRN Cell Biology

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Type III secretion systems are molecular machines used by many Gram-negative bacterial pathogens to inject proteins, known as effectors, directly into eukaryotic host cells. These proteins manipulate host signal transduction pathways and cellular processes to the pathogen's advantage. Salmonella enterica possesses two virulence-related type III secretion systems that deliver more than forty effectors. This paper reviews our current knowledge about the functions, biochemical activities, host targets, and impact on host cells of these effectors. First, the concerted action of effectors at the cellular level in relevant aspects of the interaction between Salmonella and its hosts is analyzed. Then, particular issues that will drive research in the field in the near future are discussed. Finally, detailed information about each individual effector is provided.

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“…These datasets contained 62 host-pathogen interactions for 21 S. enterica proteins [12] and 223 interactions for 69 Y. pestis proteins [13]. An initial orthology-based approach to retrieve annotations proved too restrictive and did not generate any novel insights into B. mallei virulence.…”

Section: Resultsmentioning

confidence: 99%

Mining Host-Pathogen Protein Interactions to Characterize Burkholderia mallei Infectivity Mechanisms

et al. 2015

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Burkholderia pathogenicity relies on protein virulence factors to control and promote bacterial internalization, survival, and replication within eukaryotic host cells. We recently used yeast two-hybrid (Y2H) screening to identify a small set of novel Burkholderia proteins that were shown to attenuate disease progression in an aerosol infection animal model using the virulent Burkholderia mallei ATCC 23344 strain. Here, we performed an extended analysis of primarily nine B. mallei virulence factors and their interactions with human proteins to map out how the bacteria can influence and alter host processes and pathways. Specifically, we employed topological analyses to assess the connectivity patterns of targeted host proteins, identify modules of pathogen-interacting host proteins linked to processes promoting infectivity, and evaluate the effect of crosstalk among the identified host protein modules. Overall, our analysis showed that the targeted host proteins generally had a large number of interacting partners and interacted with other host proteins that were also targeted by B. mallei proteins. We also introduced a novel Host-Pathogen Interaction Alignment (HPIA) algorithm and used it to explore similarities between host-pathogen interactions of B. mallei, Yersinia pestis, and Salmonella enterica. We inferred putative roles of B. mallei proteins based on the roles of their aligned Y. pestis and S. enterica partners and showed that up to 73% of the predicted roles matched existing annotations. A key insight into Burkholderia pathogenicity derived from these analyses of Y2H host-pathogen interactions is the identification of eukaryotic-specific targeted cellular mechanisms, including the ubiquitination degradation system and the use of the focal adhesion pathway as a fulcrum for transmitting mechanical forces and regulatory signals. This provides the mechanisms to modulate and adapt the host-cell environment for the successful establishment of host infections and intracellular spread.

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The current Salmonella‐host interactome

Cited by 57 publications

References 116 publications

Salmonella Pathogenicity and Host Adaptation in Chicken-Associated Serovars

Salmonella Pathogenicity and Host Adaptation in Chicken-Associated Serovars

Impact ofSalmonella entericaType III Secretion System Effectors on the Eukaryotic Host Cell

Mining Host-Pathogen Protein Interactions to Characterize Burkholderia mallei Infectivity Mechanisms

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