Identification of an Acinetobacter baumannii Zinc

 Acquisition System that Facilitates Resistance to

 Calprotectin-mediated Zinc Sequestration

M. Indriati Hood et al., PLoS Pathog. 2012, 8 : e1003068.

Speaker: Zih-Cian Su(蘇資茜)                                             Time: 14:00~15:00, Mar. 13, 2013

Commentator: Dr. Shu-Ying Wang (王淑鶯 老師)            Location: Room 601

Abstract

Acinetobacter baumannii is an opportunistic pathogen that has emerged as a prevalent source of nosocomial infections, most frequently causing ventilator-associated pneumonia. The emergence of pan-drug resistant strains magnifies the problem by reducing viable treatment options and effectively increasing the mortality rate associated with Acinetobacter infections. Clearly, it is imperative to develop new antimicrobial strategies to combat this emerging threat. Transition metals are involved in many crucial biological processes and are therefore necessary for the survival of all living organisms. Mn²⁺ and Zn²⁺ also have vital roles in bacteria. Mn²⁺ serves a catalytic role in many proteins and is important in resistance to oxidative stress. Zn²⁺ is abundant transition metal in most living systems and can serve catalytic and structural roles within proteins. In fact, it is estimated that Zn²⁺‑binding proteins represent approximately 4–8% of all proteins encoded in the genomes of bacteria and archaea. According to previous studies, the transport of Zn²⁺ across the outer membrane through specific receptor may be an energy-dependent process powered by theTonB–ExbB–ExbD system of inner membrane in Gram negative bacteria. In this study, authors not only identified the Zn uptake system in Acinetobacter baumannii but also demonstrated that it is required for the uptake of Zn duringpathogenesis. Furthermore, a host antimicrobial protein,calprotectin(S100A9), chelates Zn to defend Acinetobacter baumannii infection both in vitro and in vivo. In addition, carbapenem resistance was reversed by chelating Zn. A combination of limiting Zn acquisition with existing antimicrobial compounds may provide a viable strategy againstAcinetobacter baumannii.

References

1.      Hood MI. et al. Nutritional immunity: transition metals at the pathogen host interface. Nat Rev Microbiol 10: 525–37.