Zinc is an important inter-kingdom signal between the host and microbe

Abstract

Zinc (Zn) is an essential trace element in living organisms and plays a vital role in the regulation of both microbial virulence and host immune responses. A growing number of studies have shown that zinc deficiency or the internal Zn concentration does not meet the needs of animals and microbes, leading to an imbalance in zinc homeostasis and intracellular signalling pathway dysregulation. Competition for zinc ions (Zn2+) between microbes and the host exists in the use of Zn2+ to maintain cell structure and physiological functions. It also affects the interplay between microbial virulence factors and their specific receptors in the host. This review will focus on the role of Zn in the crosstalk between the host and microbe, especially for changes in microbial pathogenesis and nociceptive neuron-immune interactions, as it may lead to new ways to prevent or treat microbial infections.

dSeqSb: A systems biology approach to decipher dynamics of host-pathogen interactions using temporal dual RNA-seq data

“…Metal ions are essential for living organisms and play a vital role in the regulation of both microbial virulence and host immune responses. Recent studies have shown a role for metal ions in protection of the host against infections (84)(85)(86)(87). Therefore, it could be beneficial for the invading pathogen to express a variety of such genes in order to steal metal ions from the host.…”

Strategies for Zinc Uptake in Pseudomonas aeruginosa at the Host–Pathogen Interface

“…Bacterial competition for zinc ions (Zn 2+ ) exists as Zn 2+ is used by bacteria to maintain cell structure and physiological functions. It also affects the interplay between bacterial virulence factors and pathogenic processes ( Xia et al, 2021 ). For instance, most bacterial pathogens use zinc-dependent microbial metalloproteinases to facilitate the destruction of physiological barriers during host invasion by pathogens, thereby assisting in the pathogenesis ( Rahman and Karim, 2017 ).…”

“…Upon infection in healthy organisms, host cells use members of the ZIP transporter family to introduce Zn 2+ into the cells to prevent the proliferation and infection of pathogens. Zn 2+ is then distributed to the intracellular organelles or binds to MT through ZnT family proteins to limit the concentration of intracellular Zn 2+ ( Figure 1 ; Djoko et al, 2015 ; Xia et al, 2021 ). During this process, zinc is redistributed to various tissues such as the liver, resulting in decreased serum zinc levels.…”

“…Calprotectin (also known as S100A8/S100A9, calgranulin A/B, MRP8/14) is a heterodimer of S100A8 and S100A9 and a bivalent metal-binding protein released by neutrophils ( Gebhardt et al, 2006 ) that was originally identified based on its ability to inhibit the growth of a variety of fungal and bacterial pathogens in vitro ( Sohnle et al, 1991 ; Cassat and Skaar, 2012 ). Upon pathogen attack, calprotectin, which is one of the most abundant antibacterial proteins in neutrophils, is recruited to chelate zinc ions at the site of infection ( Xia et al, 2021 ). This chelation is mediated through two high-affinity binding sites, both of which can bind Zn 2+ with nanomolar affinity ( Kehl-Fie et al, 2011 ).…”

“…In addition to their metal-chelating properties, psoriasin, calprotectin, and calgranulin C can bind to and activate cell surface receptors, such as Toll-like receptor 4 (TLR4), receptor for advanced glycation end-products (RAGE), and G protein-coupled receptors (GPCRs) to initiate intracellular inflammatory signal transduction. These proteins also play an important role in the regulation of immune and inflammatory responses ( Carvalho et al, 2020 ; Xia et al, 2021 ).…”