Metallobiology of host–pathogen interactions: an intoxicating new insight

Botella, Hélène; Stadthagen, Gustavo; Lugo-Villarino, Geanncarlo; Chastellier, Chantal de; Neyrolles, Olivier

doi:10.1016/j.tim.2012.01.005

Cited by 104 publications

(96 citation statements)

References 54 publications

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“…This inactivation may lead to the accumulation of the non-acylated mycobactin core, which could be either degraded by a siderophore esterase, even though none has yet been identified in M. tuberculosis, or be used as intracellular ion storage molecule. Recently, it was shown that the host increases the macrophage vacuole concentration of zinc and copper, as a novel immune response, to "poison" the bacteria with metal ions (35,36). It is reasonable to speculate that M. tuberculosis, in addition to specific metal efflux pumps, is using the mycobactin or the mycobactin core to neutralize excess copper and zinc as seen in Pseudomonas aeruginosa (37) and pathogenic strains of E. coli (38).…”

Section: Discussionmentioning

confidence: 99%

Mechanism and Regulation of Mycobactin Fatty Acyl-AMP Ligase FadD33

Vergnolle

Blanchard

2013

Journal of Biological Chemistry

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Background: Fatty acyl-AMP ligase FadD33 is required for mycobactin biosynthesis. Results: FadD33 catalyzes a two-step kinetic mechanism, and FadD33 activity is regulated by post-translational acetylation. Conclusion: Mycobactin FadD33 activity is reversibly regulated by Pat (acetylation) and DAc1 (deacetylation). Significant: Post-translational regulation via acetylation of enzymes can modulate siderophore biosynthesis.

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Section: Discussionmentioning

confidence: 99%

Mechanism and Regulation of Mycobactin Fatty Acyl-AMP Ligase FadD33

Vergnolle

Blanchard

2013

Journal of Biological Chemistry

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“…Macrophages can deprive Histoplasma capsulatum of zinc by reducing the phagosome zinc content [91]. On the other hand, they kill Mycobacterium tuberculosis by intoxicating it with excess amounts of zinc and copper [92].…”

Section: Zinc In Infection a Nutritional Immunitymentioning

confidence: 99%

Zinc in Infection and Inflammation

Gammoh¹,

Rink²

2017

Preprint

187

139

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Abstract:Micronutrient homeostasis is a key factor in maintaining a healthy immune system. Zinc is an essential micronutrient that is involved in the regulation of the innate and adaptive immune responses. The main cause of zinc deficiency is malnutrition. Zinc deficiency leads to cell-mediated immune dysfunctions among other manifestations. Consequently, such dysfunctions lead to a worse outcome in the response towards bacterial infection and sepsis. For instance, zinc is an essential component of the pathogen-eliminating signal transduction pathways leading to neutrophil extracellular traps formation, as well as inducing cell-mediated immunity over humoral immunity by regulating specific factors or differentiation. Additionally, zinc deficiency plays a role in inflammation, mainly elevating inflammatory response as well as damage to host tissue. Zinc is involved in the modulation of the proinflammatory response by targeting Nuclear Factor Kappa B, a transcription factor that is the master regulator of proinflammatory responses. It is also involved in controlling oxidative stress and regulating inflammatory cytokines. Zinc plays an intricate function during an immune response and its homeostasis is critical for sustaining proper immune function. This review will summarize the latest findings concerning the role of this micronutrient during the course of infections and inflammatory response and how the immune system modulates zinc depending on different stimuli.

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“…The mechanisms of copper homeostasis in mycobacteria include copper efflux and sequestration of cytoplasmic copper by the metallothionein MymT (13,(17)(18)(19). Multicopper oxidases play a crucial role in copper detoxification in many bacteria, including Escherichia coli (20), Pseudomonas syringae (21), Salmonella enterica (22), and others (23,24).…”

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confidence: 99%