Effects of Fine Particulate Matter onPseudomonas aeruginosaAdhesion and Biofilm FormationIn Vitro

Abstract

Respiratory infections of Pseudomonas aeruginosa are a major cause of mortality and morbidity for hospitalized patients. Fine particulate matter (FPM) is known to have interactions with some bacterial infection in the respiratory system. In this report, we investigate the effect of different concentration of FPM on P. aeruginosa attachment and biofilm formation using in vitro cell culture systems. P. aeruginosa were cultured to form mature biofilms on hydroxyapatite-coated peg and the number of bacteria in the biofilms was enumerated. Morphology of biofilm was imaged with scanning electron microscopy and confocal laser scanning microscopy. Bacterial affinity change to the cell membrane was evaluated with attached colony counting and fluorescence microscopy images. Alteration of bacterial surface hydrophobicity and S100A4 protein concentration were explored as mechanisms of P. aeruginosa adhesion to human cells. There were a concentration-dependent increase of thickness and surface roughness of biofilm mass. P. aeruginosa adherence to respiratory epithelial cells was increased after FPM treatment. Bacterial surface hydrophobicity and S1000A4 protein concentration were increased with proportionally the dose of FPM in media. FPM in the airway could enhance both the adhesion of P. aeruginosa to epithelial cells and biofilm formation. Bacterial surface hydrophobicity and human cell plasma membrane injury are associated with binding of P. aeruginosa on airway epithelial cells and biofilm formation.

Air pollution induces Staphylococcus aureus USA300 respiratory tract colonization mediated by specific bacterial genetic responses involving the global virulence gene regulators Agr and Sae

“…In this study we show that simultaneous inoculation of S. aureus and biologically relevant concentrations of BC causes increased infection of murine lungs and increased nasopharyngeal colonization. These new data agree with our previous observations with S. pneumoniae exposed to BC (Hussey et al, 2017) and confirm a wider phenomenon of the impact of BC on bacterial respiratory tract colonization, that also been recently shown with other types of particulate pollutant (Liu et al, 2019;Shears et al, 2020;Woo et al, 2018;Yadav et al, 2020).…”

Air pollution induces Staphylococcus aureus USA300 respiratory tract colonisation mediated by specific bacterial genetic responses dependent on the global virulence gene regulators Agr and Sae

“…In this study we show that simultaneous inoculation of S. aureus and biologically relevant concentrations of BC causes increased infection of murine lungs and increased nasopharyngeal colonisation. These new data agree with our previous observations with S. pneumoniae exposed to BC (Hussey et al, 2017) and confirms a wider phenomenon of the impact of BC on bacterial respiratory tract colonisation, that also been recently shown with other types of particulate pollutant (Liu et al, 2019; Shears et al, 2020; Woo et al, 2018; Yadav et al, 2020).…”

“…To our knowledge, this is the first study to pre-grow the bacteria with PM prior to inoculation. All previous studies have either pre-exposed the host to PM or inoculated PM and bacteria together(Liu et al, 2019; Shears et al, 2020; Woo et al, 2018; Yadav et al, 2020). These publications hypothesised that increased bacterial colonisation was due to PM binding to the bacteria thereby promoting transmission throughout the respiratory tract, or PM providing metabolites to support bacterial growth or PM-mediated toxicity damaging epithelial integrity (Liu et al ., 2019; Yadav et al ., 2020; Shears et al ., 2020).…”

“…The instillation of BC into the mice did not cause detectable tissue damage, indicating that BC acts as a signal that alters bacterial behaviour (Hussey et al, 2017). Subsequent studies also showed that direct bacterial exposure to a variety of PM sources also increased biofilm formation (Woo et al, 2018; Yadav et al, 2020) and increased S. pneumoniae nasopharyngeal colonisation and dissemination to the lungs and middle ear of mice (Yadav et al, 2020). None of these studies sought to determine the biological mechanisms involved in the bacterial response to PM exposure, but the BC-induced changes could be a key contributing factor in how air pollutants cause increased lower respiratory tract infectious disease.…”

The Impact of PM2.5 on the Host Defense of Respiratory System

“…In addition, Liu et al (2018) reported that ROS induced by PM 2.5 activated the AKT/STAT3/NF-κB pathway through IL-6 paracrine signaling, which then upregulated the expression of intercellular adhesion molecule-1 (ICAM-1, an important glycoprotein on the cell surface) in the lung to increase the adhesion of pathogens to the airway epithelium (Figure 3B). Woo et al (2018) also found that PM 2.5 could enhance the adhesion of P. aeruginosa to epithelial cells, the mechanism of which depended on the increased bacterial surface hydrophobicity and damaged human cell plasma membrane by PM 2.5 . Tight junctions (TJs) are the significant protein complexes at cell-cell interfaces that connect adjacent cells with each other to form lung epithelial barrier against pathogens (Schlingmann et al, 2015).…”