Wall Teichoic Acids of Staphylococcus aureus Limit Recognition by the Drosophila Peptidoglycan Recognition Protein-SA to Promote Pathogenicity

Atilano, Magda L.; Yates, James R.; Glittenberg, Marcus; Filipe, Sérgio R.; Ligoxygakis, Petros

doi:10.1371/journal.ppat.1002421

Cited by 46 publications

(54 citation statements)

References 49 publications

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“…Therefore, crq ko flies are susceptible to Gram-positive bacteria and fungal infections and strongly susceptible to infection with S . aureus , a bacterium specifically cleared by phagocytosis [19,62,63]. …”

Section: Resultsmentioning

confidence: 99%

The Drosophila CD36 Homologue croquemort Is Required to Maintain Immune and Gut Homeostasis during Development and Aging

et al. 2016

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Phagocytosis is an ancient mechanism central to both tissue homeostasis and immune defense. Both the identity of the receptors that mediate bacterial phagocytosis and the nature of the interactions between phagocytosis and other defense mechanisms remain elusive. Here, we report that Croquemort (Crq), a Drosophila member of the CD36 family of scavenger receptors, is required for microbial phagocytosis and efficient bacterial clearance. Flies mutant for crq are susceptible to environmental microbes during development and succumb to a variety of microbial infections as adults. Crq acts parallel to the Toll and Imd pathways to eliminate bacteria via phagocytosis. crq mutant flies exhibit enhanced and prolonged immune and cytokine induction accompanied by premature gut dysplasia and decreased lifespan. The chronic state of immune activation in crq mutant flies is further regulated by negative regulators of the Imd pathway. Altogether, our data demonstrate that Crq plays a key role in maintaining immune and organismal homeostasis.

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Section: Resultsmentioning

confidence: 99%

The Drosophila CD36 Homologue croquemort Is Required to Maintain Immune and Gut Homeostasis during Development and Aging

et al. 2016

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“…For example, changes in PG composition and altered PG synthase activity contribute to bile resistance in Salmonella enterica (39,41) and PG composition changes during stationary phase (42). Pathogenic bacteria can also remodel PG to avoid a host response (5,(43)(44)(45)(46). Previous studies have shown that the number and activity of PG synthetic enzymes and their interaction partners vary significantly in different organisms (47).…”

Section: Discussionmentioning

confidence: 99%

Cell Separation in Vibrio cholerae Is Mediated by a Single Amidase Whose Action Is Modulated by Two Nonredundant Activators

et al. 2014

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Synthesis and hydrolysis of septal peptidoglycan (PG) are critical processes at the conclusion of cell division that enable separation of daughter cells. Cleavage of septal PG is mediated by PG amidases, hydrolytic enzymes that release peptide side chains from the glycan strand. Most gammaproteobacteria, including Escherichia coli, encode several functionally redundant periplasmic amidases. However, members of the Vibrio genus, including the enteric pathogen Vibrio cholerae, encode only a single PG amidase, AmiB. Here, we show that V. cholerae AmiB is crucial for cell division and growth. Genetic and biochemical analyses indicated that AmiB is regulated by two activators, EnvC and NlpD, at least one of which is required for AmiB's localization to the cell division site. Localization of the activators (and thus of AmiB) is dependent upon the cell division protein FtsN. These factors mediate septal PG cleavage in E. coli as well; however, their precise roles vary between the two organisms in a number of ways. Notably, even though V. cholerae EnvC and NlpD appear to be functionally redundant under most growth conditions tested, NlpD is specifically required for intestinal colonization in the infant mouse model of cholera and for V. cholerae resistance against bile salts, perhaps due to environmental regulation of AmiB or its activators. Collectively, our findings reveal that although the cellular components that enable cleavage of septal PG appear to be generally conserved between E. coli and V. cholerae, they can be combined into diverse functional regulatory networks.

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“…Lysosome can kill bacteria through cell wall degradation, which further generates peptidoglycan (PPG) fragments that can be recognized by pattern-recognition receptors (PRRs, see sidebar) such as NOD2 (35) and peptidoglycan recognition protein (25). Gram-positive pathogens have evolved mechanisms to PPG less recognizable to lysozyme, including PPG modification in SPN (122) and GAS (41), O -acetylation in SPN (32) and S. aureus (11), and masking of PPG with covalently linked wall teichoic acid (WTA) structures in S. aureus (8). Functionally, modification of PPG to impart lysozyme resistance results in not only evasion of detection by PRRs, but also limiting of host production of important inflammatory mediators such as interleukin (IL)-1β via the Nod-like receptor (NLR) family pyrin-domain-containing 3 (NLRP3) inflammasome (see sidebar) and interferon-β (64, 109).…”

Section: Resistance To Phagocytic Granule Componentsmentioning

confidence: 99%

Subterfuge and Sabotage: Evasion of Host Innate Defenses by Invasive Gram-Positive Bacterial Pathogens

Okumura

Nizet

2014

Annu. Rev. Microbiol.

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The development of a severe invasive bacterial infection in an otherwise healthy individual is one of the most striking and fascinating aspects of human medicine. A small cadre of gram-positive pathogens of the genera Streptococcus and Staphylococcus stand out for their unique invasive disease potential and sophisticated ability to counteract the multifaceted components of human innate defense. This review illustrates how these leading human disease agents evade host complement deposition and activation, impede phagocyte recruitment and activation, resist the microbicidal activities of host antimicrobial peptides and reactive oxygen species, escape neutrophil extracellular traps, and promote and accelerate phagocyte cell death through the action of pore-forming cytolysins. Understanding the molecular basis of bacterial innate immune resistance can open new avenues for therapeutic intervention geared to disabling specific virulence factors and resensitizing the pathogen to host innate immune clearance.

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Wall Teichoic Acids of Staphylococcus aureus Limit Recognition by the Drosophila Peptidoglycan Recognition Protein-SA to Promote Pathogenicity

Cited by 46 publications

References 49 publications

The Drosophila CD36 Homologue croquemort Is Required to Maintain Immune and Gut Homeostasis during Development and Aging

The Drosophila CD36 Homologue croquemort Is Required to Maintain Immune and Gut Homeostasis during Development and Aging

Cell Separation in Vibrio cholerae Is Mediated by a Single Amidase Whose Action Is Modulated by Two Nonredundant Activators

Subterfuge and Sabotage: Evasion of Host Innate Defenses by Invasive Gram-Positive Bacterial Pathogens

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