A chronic strain of the cystic fibrosis pathogen Pandoraea pulmonicola expresses a heterogenous hypo-acylated lipid A
- PDF / 1,412,975 Bytes
- 10 Pages / 595.276 x 790.866 pts Page_size
- 33 Downloads / 133 Views
ORIGINAL ARTICLE
A chronic strain of the cystic fibrosis pathogen Pandoraea pulmonicola expresses a heterogenous hypo-acylated lipid A Molly D. Pither 1 & Siobhán McClean 2,3
&
Alba Silipo 1
&
Antonio Molinaro 1
&
Flaviana Di Lorenzo 1
Received: 31 July 2020 / Revised: 16 September 2020 / Accepted: 7 October 2020 # The Author(s) 2020
Abstract Pandoraea sp. is an emerging Gram-negative pathogen in cystic fibrosis causing severe and persistent inflammation and damage of the lungs. The molecular mechanisms underlying the high pathogenicity of Pandoraea species are still largely unknown. As Gram-negatives, Pandoraea sp. express lipopolysaccharides (LPS) whose recognition by the host immune system triggers an inflammatory response aimed at the bacterial eradication from the infected tissues. The degree of the inflammatory response strongly relies on the fine structure of the LPS and, in particular, of its glycolipid moiety, i.e. the lipid A. Here we report the structure of the lipid A isolated from the LPS of a chronic strain of P. pulmonicola (RL 8228), one of the most virulent identified so far among the Pandoraea species. Our data demonstrated that the examined chronic strain produces a smooth-type LPS with a complex mixture of hypoacylated lipid A species displaying, among other uncommon characteristics, the 2-hydroxylation of some of the acyl chains and the substitution by an additional glucosamine on one or both the phosphate groups. Keywords Lipopolysaccharide . Cystic Fibrosis . Pandoraea . Lipid A . Structural characterization . MALDI-TOF Mass spectrometry
Introduction Cystic fibrosis (CF) is an incurable, chronic disease, caused by defects in genes encoding for the CF transmembrane conductance regulator (CFTR), a chloride channel which regulates the activity of other chloride and sodium channels at the cell surface epithelium [1]. Defective CFTR results in abnormal movement of salts and water across the cells which leads to dehydration of the airway surfaces and production of a thick and sticky mucus obstructing the pathways. This clog of the airways leads to breathing problems and to repeated and Electronic supplementary material The online version of this article (https://doi.org/10.1007/s10719-020-09954-8) contains supplementary material, which is available to authorized users. * Flaviana Di Lorenzo [email protected] 1
Department of Chemical Sciences, University of Naples Federico II, via Cinthia 4, Naples 80126, Italy
2
Centre of Microbial Host Interactions, Institute of Technology Tallaght, Dublin 24, Ireland
3
School of Biomolecular and Biomedical Sciences, University College Dublin, Belfield, Dublin 4, Ireland
serious lung infections with damaging inflammation [2]. Indeed, the main cause of morbidity and mortality for CF patients is associated to infection by bacterial pathogens and opportunistic pathogens encountered throughout their lives. Beside Pseudomonas aeruginosa and bacteria of the Burkholderia cepacia complex, which are well-known Gram-negative opportunistic pathogens
Data Loading...
