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- W4312230887 abstract "<b>Background:</b> Non-typeable Haemophilus influenzae (NTHi) is the most common lower respiratory tract bacterium. It causes persistent infections, neutrophilic inflammation and promotes exacerbations in asthma and COPD. Internalisation of NTHi into the epithelium may promote persistence and trigger immune activation. <b>Methods:</b> BEAS-2B, Calu-3, and RPMI2650 cell lines, and healthy primary bronchial or nasal epithelial cells were cocultured with NTHi. Adherent, paracellular and internalised bacteria were enumerated by gentamicin exclusion assays. Signalling pathways were evaluated by qPCR, and IL-8 production was confirmed by ELISA. <b>Results:</b> In cell lines and primary cells, differing internalisation rates between NTHi strains did not correlate with induction of IL-6, -8, CCL2, TNF and NLRP3 inflammasome marker IL-1b. Cytochalasin diminished IL-1b production but did not affect other cytokines. Intracellular NTHi localised within the late endosome of secretory and basal cells, but viable bacilli did not persist beyond 48 h in cell lines or 24 h in primary cells. In primary cells at air-liquid interface culture there was more upregulation of TLR signalling (IRF5, TRAF-6, RelA, ALPK1), NOD signalling (NOD1, NOD2, MPAK3, MAPK8) and of ICAM1, Caspase1 and IL-8 in nasal epithelial cells than lower airway bronchial cells. <b>Conclusions:</b> NTHi potently induces a bronchial epithelial innate response, independent of internalisation rate with limited NLRP3 dependence, implicating surface immune sensing via TLR2 and 4. Increased inflammatory signalling in the lower airways is not due to increased innate immune responsiveness of bronchial epithelial cells." @default.
- W4312230887 created "2023-01-04" @default.
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- W4312230887 date "2022-09-04" @default.
- W4312230887 modified "2023-09-23" @default.
- W4312230887 title "Non-typeable Haemophilus influenzae activates respiratory epithelial cell innate immune responses independently of intracellular internalisation" @default.
- W4312230887 doi "https://doi.org/10.1183/13993003.congress-2022.2067" @default.
- W4312230887 hasPublicationYear "2022" @default.
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