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Haemophilus influenzae responds to the steroid beclomethasone used in asthma therapy by modulation of biofilm formation and antibiotic tolerance

ABSTRACT: Haemophilus influenzae responds to the steroid beclomethasone used in asthma therapy by modulation of biofilm formation and antibiotic tolerance

ORGANISM(S): Haemophilus influenzae Rd KW20

PROVIDER: GSE125415 | GEO | 2019/06/30

REPOSITORIES: GEO

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Haemophilus influenzae responds to the steroid beclomethasone used in asthma therapy by modulation of biofilm formation and antibiotic tolerance

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Project description:Asthma is the most common chronic respiratory disease. Asthma that cannot be well controlled by steroid treatment is called steroid-resistant asthma. Steroid-resistant asthma accounts for only 5% of all asthma cases, but it accounts for 80% of asthma healthcare costs. Nontypeable Haemophilus influenzae (NTHi), as a Gram-negative bacterium, can release outer membrane vesicles (OMVs) and transfer biomolecules to host cells and the external environment by carrying lipopolysaccharides, proteins, peptidoglycans, outer membrane proteins, cell wall components, proteins, nucleic acids, ion metabolites, and signaling molecules. Thus, it plays a role in obtaining nutrition, stress, toxin delivery, adhesion, host immune surveillance evasion, and host immune response regulation. It becomes an essential way in bacterial pathogenesis. To further clarify whether NTHi OMVs could be inhaled to induce steroid-resistant asthma, we isolated and purified NTHi OMVs. In vivo experiments showed that NTHi OMVs could be inhaled and enter airway epithelial cells. Cosensitization with OVA induces steroid-resistant asthma in mice. Furthermore, through high-throughput sequencing, we found that the NTHi OMVs and OVA co-sensitized mice had significantly enriched inflammatory and immune-related signaling pathways, and the transcription and secretion of IL-1β were increased was the potential cause of SRA.

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Project description:Glucocorticosteroids are used as a main treatment to reduce airway inflammation in people with asthma who suffer from neutrophilic airway inflammation, a condition frequently associated with Haemophilus influenzae colonization. Here we show that glucocorticosteroids have a direct influence on the behavior of H. influenzae that may account for associated difficulties with therapy. Using a mouse model of infection, we show that corticosteroid treatment promotes H. influenzae persistence. Transcriptomic analysis of bacteria either isolated from infected mouse airway or grown in laboratory medium identified a number of genes encoding regulatory factors whose expression responded to the presence of glucocorticosteroids. Importantly, a number of these corticosteroid-responsive genes also showed elevated expression in H. influenzae within sputum from asthma patients undergoing steroid treatment. Addition of corticosteroid to H. influenzae led to alteration in biofilm formation and enhanced resistance to azithromycin, and promoted azithromycin resistance in an animal model of respiratory infection. Taken together, these data strongly suggest that H. influenzae can respond directly to corticosteroid treatment in the airway potentially influencing biofilm formation, persistence and the efficacy of antibiotic treatment.

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Retraction: "Haemophilus influenzae responds to glucocorticoids used in asthma therapy by modulation of biofilm formation and antibiotic resistance".

Project description:Chris S Earl, Teh Wooi Keong, Shi-qi An, Sarah Murdoch, Yvonne McCarthy, Junkal Garmendia, Joseph Ward, J Maxwell Dow, Liang Yang, George A O'Toole & Robert P RyanThe above article, published May 20 2015 in EMBO Molecular Medicine, has been retracted by agreement between the authors of the study, CSE, TWK, SQA, SM, YMcC, JG, JW, JMD, LY, RPR, the journal Chief Editor and the EMBO Head of Scientific Publications in accordance with the outcomes of independent investigations conducted by the University of Dundee and University College Cork.GAO'T disagrees with the text of this retraction notice, albeit not with the retraction.The following issues are noted: Table 1 contains clinical data described in the paper as being derived from a cohort of asthma patients. However, the provenance of this data is unclear. Based on the evidence available, the University of Dundee investigation concluded that the majority of the patient cohort is likely to be a subset of a cohort of cystic fibrosis patients reported in PLoS One 8(12): e82432 (https://doi.org/10.1371/journal.pone.0082432), although in a number of cases the patient's gender is at odds between the two reports.The RNAseq data are unavailable on the European Nucleotide Archive under the reported accession number ERG003569. RNAseq data were uploaded with accession number ERS654066 before publication.The paper describes use of both prednisolone and prednisone, yet only the latter was used in the study.

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