Willem J Wiersinga1, Tom van der Poll. 1. Center for Infection and Immunity Amsterdam, Center for Experimental and Molecular Medicine and Department of Medicine, Academic Medical Center, Meibergdreef 9, Amsterdam, the Netherlands. w.j.wiersinga@amc.uva.nl
Abstract
PURPOSE OF REVIEW: Largely due to its recognition as a biological threat agent, current knowledge on melioidosis, caused by the Gram-negative bacterium Burkholderia pseudomallei, has increased tremendously over the last years. This review summarizes current understanding on the molecular characterization of B. pseudomallei and the immunology of melioidosis. RECENT FINDINGS: The genome of B. pseudomallei is composed of two chromosomes of which the largest part represents the B. pseudomallei core genome, whereas the remaining accessory genome has been associated with bacterial virulence. Virulence factors, most notably quorum sensing, type III secretion system, lipopolysaccharide and other surface polysaccharides, flagella and various factors essential for the intracellular life cycle of B. pseudomallei, have been further characterized. The neutrophils play a critical in host defense, which is initiated by the Toll-like receptors. The proinflammatory immune response--including the activation of coagulation-- and its regulation have been further dissected. SUMMARY: Severe melioidosis can probably be seen as the clinical manifestation of a pathogen recognition receptor mediated dysregulation of the immune response to invading B. pseudomallei. B. pseudomallei employs numerous tactics to evade the immune response. Studies on host-pathogen interactions in melioidosis have identified a whole range of potential new treatment targets.
PURPOSE OF REVIEW: Largely due to its recognition as a biological threat agent, current knowledge on melioidosis, caused by the Gram-negative bacterium Burkholderia pseudomallei, has increased tremendously over the last years. This review summarizes current understanding on the molecular characterization of B. pseudomallei and the immunology of melioidosis. RECENT FINDINGS: The genome of B. pseudomallei is composed of two chromosomes of which the largest part represents the B. pseudomallei core genome, whereas the remaining accessory genome has been associated with bacterial virulence. Virulence factors, most notably quorum sensing, type III secretion system, lipopolysaccharide and other surface polysaccharides, flagella and various factors essential for the intracellular life cycle of B. pseudomallei, have been further characterized. The neutrophils play a critical in host defense, which is initiated by the Toll-like receptors. The proinflammatory immune response--including the activation of coagulation-- and its regulation have been further dissected. SUMMARY: Severe melioidosis can probably be seen as the clinical manifestation of a pathogen recognition receptor mediated dysregulation of the immune response to invading B. pseudomallei. B. pseudomallei employs numerous tactics to evade the immune response. Studies on host-pathogen interactions in melioidosis have identified a whole range of potential new treatment targets.
Authors: John J Yeager; Paul Facemire; Paul A Dabisch; Camenzind G Robinson; David Nyakiti; Katie Beck; Reese Baker; M Louise M Pitt Journal: Infect Immun Date: 2012-07-09 Impact factor: 3.441
Authors: Laura Conejero; Natasha Patel; Melanie de Reynal; Sara Oberdorf; Joanne Prior; Philip L Felgner; Richard W Titball; Francisco J Salguero; Gregory J Bancroft Journal: Am J Pathol Date: 2011-05-05 Impact factor: 4.307
Authors: Muhammad R A Hassan; Subhada P Pani; Ng P Peng; Kirtanaa Voralu; Natesan Vijayalakshmi; Ranjith Mehanderkar; Norasmidar A Aziz; Edwin Michael Journal: BMC Infect Dis Date: 2010-10-21 Impact factor: 3.090
Authors: Gerritje J W van der Windt; W Joost Wiersinga; Catharina W Wieland; Ivo C S I Tjia; Nicholas P Day; Sharon J Peacock; Sandrine Florquin; Tom van der Poll Journal: PLoS Negl Trop Dis Date: 2010-08-31