PT  - JOURNAL ARTICLE
AU  - Miyashita, Lisa
AU  - Coldwell, Beverley
AU  - Wertheim, David
AU  - Gill, Ian
AU  - Crust, Simon
AU  - M. Pérez, Nemesio
AU  - Petford, Nick
AU  - Grigg, Jonathan
TI  - Sand Particles Increase Pneumococcal Adhesion to Respiratory cells in vitro
AID  - 10.1183/13993003.congress-2023.PA1104
DP  - 2023 Sep 09
TA  - European Respiratory Journal
PG  - PA1104
VI  - 62
IP  - suppl 67
4099  - http://erj.ersjournals.com/content/62/suppl_67/PA1104.short
4100  - http://erj.ersjournals.com/content/62/suppl_67/PA1104.full
SO  - Eur Respir J2023 Sep 09; 62
AB  - Background: Studies have suggested that there can be increases in respiratory disease in Europe associated with sandstorms originating from the Sahara, sometimes known as Calima sandstorm events (1, 2). We previously showed that volcanic ash particles increase susceptibility to pneumococcal infection (3).Aim: Assess effect of as Calima sandstorm particles on pneumococcal adhesion to A549 alveolar epithelial cells in vitro.Methods: Airborne mineral dust originating in Saharan Africa and deposited on Tenerife during a sandstorm (Calima event, February 2020) were collected. Samples were filtered (10 mm mesh), suspended in DPBS and added to adherent A549 lung epithelial cells (2x105 cells/well) in cell culture plates for 2h. After washing, D39 S. pneumoniae strain was incubated with cells for 2h. Cells were washed and lysed before adherent bacteria were enumerated on blood agar plates for colony forming units (CFU) counts. PAFR expression assessed by flow cytometry.Results: Incubation with Calima particles (10mg/ml) increased pneumococcal adhesion to A549 lung epithelial cells (figure, n=6, mean±SEM 1637±/173.8ml vs 2467±252.8/ml, *P<0.05).Conclusion: Camila Sand particles increases pneumococcal adherence to airway cells in vitro.References: (1) Karanasiou A et al., Oct 15;47:107-14. doi: 10.1016/j.envint.2012.06.012.(2) López-Villarrubia E, et al., 2021 Jul;57(7):464-470. doi: 10.1016/j.arbr.2020.03.032.(3) Miyashita L, et al., ERS 2022 60: 3163; DOI: 10.1183/13993003.congress-2022.3163FootnotesCite this article as: European Respiratory Journal 2023; 62: Suppl. 67, PA1104.This abstract was presented at the 2023 ERS International Congress, in session “Inflammatory endotyping: the macrophage across disease areas”.This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).