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Pro-inflammatory cytokines can act as intracellular modulators of commensal bacterial virulence.

Journal article
Authors Jafar Mahdavi
Pierre Joseph Royer
Hong S. Sjölinder
Sheyda Azimi
Tim Self
Jeroen Stoof
Lee M. Wheldon
Kristoffer Brännström
Raymond Wilson
Joanna Moreton
James W.B. Moir
Carina Sihlbom
Thomas Borén
Ann Beth Jonsson
Panos Soultanas
Dlawer A.A. Ala'Aldeen
Published in Open biology
Volume 3
Pages 130048
Publication year 2013
Published at Core Facilities, Proteomics
Pages 130048
Language en
Links doi.org/10.1098/rsob.130048
Subject categories Biological Sciences

Abstract

Interactions between commensal pathogens and hosts are critical for disease development but the underlying mechanisms for switching between the commensal and virulent states are unknown. We show that the human pathogen Neisseria meningitidis, the leading cause of pyogenic meningitis, can modulate gene expression via uptake of host pro-inflammatory cytokines leading to increased virulence. This uptake is mediated by type IV pili (Tfp) and reliant on the PilT ATPase activity. Two Tfp subunits, PilE and PilQ, are identified as the ligands for TNF-α and IL-8 in a glycan-dependent manner, and their deletion results in decreased virulence and increased survival in a mouse model. We propose a novel mechanism by which pathogens use the twitching motility mode of the Tfp machinery for sensing and importing host elicitors, aligning with the inflamed environment and switching to the virulent state.

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