Catecholamine norepinephrine diminishes lung epithelial cell adhesion of Streptococcus pneumoniae by binding iron

Microbiology
Xavier F GonzalesYolanda López-Vidal

Abstract

Systemic release of norepinephrine (NE) is a component of the acute host response to infection, and studies in the field of microbial endocrinology indicate generally that NE increases the bacterial growth rate and promotes invasive disease. However, NE attenuates experimental invasive pneumococcal disease. We determined that NE promoted pneumococcal growth but paradoxically decreased pneumococcal adhesion to host cells. This effect was independent of the classical adhesin CbpA. Microarray analysis indicated that the effect of NE involved two two-component regulatory systems that both regulate expression of the Piu iron uptake ABC transport operon. We propose that NE, a known siderophore, enhances iron availability to the bacteria, resulting in greater bacterial replication and decreased expression of Piu operon products. Downregulation of the operon includes decreased expression of the Piu-associated adhesin PiuD. Our results suggested that the iron-dependent inhibitory effect of NE on pneumococcal adherence is a mechanism underlying the amelioration of pneumococcal disease by NE.

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Citations

Sep 18, 2015·Annals of the New York Academy of Sciences·Leon Islas WeinsteinRogelio Hernandez Pando
Mar 18, 2020·Chembiochem : a European Journal of Chemical Biology·Yifan ZhangDavid P Giedroc
Jul 12, 2017·Frontiers in Cellular and Infection Microbiology·Colette G Ngo NdjomHarlan P Jones
May 1, 2021·Microorganisms·Sergey Vladislavovich Mart'yanovAndrei Vladislavovich Gannesen

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