Abstract
Particulate matter (PM) exposure is linked to the worsening of respiratory conditions, including allergic rhinitis (AR), as it can trigger nasal and systemic inflammation. To unveil the underlying molecular mechanisms, we investigated the effects of PM exposure on the release of plasmatic extracellular vesicles (EV) and on the complex cross-talk between the host and the nasal microbiome. To this aim, we evaluated the effects of PM10 and PM2.5 exposures on both the bacteria-derived-EV portion (bEV) and the host-derived EVs (hEV), as well as on bacterial nasal microbiome (bNM) features in 26 AR patients and 24 matched healthy subjects (HS). In addition, we assessed the role exerted by the bNM as a modifier of PM effects on the complex EV signaling network in the paradigmatic context of AR. We observed that PM exposure differently affected EV release and bNM composition in HS compared to AR, thus potentially contributing to the molecular mechanisms underlying AR. The obtained results represent the first step towards the understanding of the complex signaling network linking external stimuli, bNM composition, and the immune risponse.
Highlights
Exposure to particulate matter (PM) has been linked to the worsening of several respiratory allergies [1,2,3,4,5], including allergic rhinitis (AR), which affects more than 400 million people worldwide [6]
We evaluated whether the correlation matrix of the relative abundances of the genera was factorable through both visual inspections of the matrix and statistical procedures, including Bartlett’s test of sphericity, the Kaiser–Meyer–Olkin measure, and individual measures of sampling adequacy
No differences were found between AR and healthy subjects (HS) groups in any of the socio-demographic characteristics factors (Table 1)
Summary
Exposure to particulate matter (PM) has been linked to the worsening of several respiratory allergies [1,2,3,4,5], including allergic rhinitis (AR), which affects more than 400 million people worldwide [6]. The underlying mechanisms linking PM exposure and allergy remain a matter of debate [7,8,9], it is becoming increasingly clear that PM can trigger local and systemic inflammatory responses involving innate and adaptive immunity, potentially enhancing the exacerbation of allergic symptoms [10,11] In this context, plasmatic extracellular vesicles (EVs), which have a critical role in the cross-talk between cells [12,13,14], are a good candidate as mediators of the airway allergic process enhancement [15,16]. It is worthy to note that the bacterial nasal microbiome
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