Year-end Sale % OFF 
Abstract
BackgroundStudies from our laboratory have shown that human alveolar macrophages (AM) and bronchial epithelial cells (HBEC) exposed to ambient particles (PM10) in vitro increase their production of inflammatory mediators and that supernatants from PM10-exposed cells shorten the transit time of monocytes through the bone marrow and promote their release into the circulation.MethodsThe present study concerns co-culture of AM and HBEC exposed to PM10 (EHC-93) and the production of mediators involved in monocyte kinetics measured at both the mRNA and protein levels. The experiments were also designed to determine the role of the adhesive interaction between these cells via the intercellular adhesion molecule (ICAM)-1 in the production of these mediators.ResultsAM/HBEC co-cultures exposed to 100 μg/ml of PM10 for 2 or 24 h increased their levels of granulocyte-macrophage colony-stimulating factor (GM-CSF), M-CSF, macrophage inflammatory protein (MIP)-1β, monocyte chemotactic protein (MCP)-1, interleukin (IL)-6 and ICAM-1 mRNA, compared to exposed AM or HBEC mono-cultures, or control non-exposed co-cultures. The levels of GM-CSF, M-CSF, MIP-1β and IL-6 increased in co-cultured supernatants collected after 24 h exposure compared to control cells (p < 0.05). There was synergy between AM and HBEC in the production of GM-CSF, MIP-1β and IL-6. But neither pretreatment of HBEC with blocking antibodies against ICAM-1 nor cross-linking of ICAM-1 on HBEC blocked the PM10-induced increase in co-culture mRNA expression.ConclusionWe conclude that an ICAM-1 independent interaction between AM and HBEC, lung cells that process inhaled particles, increases the production and release of mediators that enhance bone marrow turnover of monocytes and their recruitment into tissues. We speculate that this interaction amplifies PM10-induced lung inflammation and contributes to both the pulmonary and systemic morbidity associated with exposure to air pollution.
Highlights
Studies from our laboratory have shown that human alveolar macrophages (AM) and bronchial epithelial cells (HBEC) exposed to ambient particles (PM10) in vitro increase their production of inflammatory mediators and that supernatants from PM10-exposed cells shorten the transit time of monocytes through the bone marrow and promote their release into the circulation
AM/HBEC co-cultures and PM10 We previously showed that the majority of AM and HBEC were in contact with each other in our co-culture system [13]
Because the RNase protection assay (RPA) kit is not provided with an internal control to account for variation between autoradiographs of different pairs of control versus PM10 treated cells such as those shown in Figure 1 and due to that fact that cells from a single but different patient are represented in each different pair, as documented by the differences in intensity of the control L32 band(s) compared to that of the corresponding glyceraldehyde-3-phosphate dehydrogenase (GAPDH) bands as well as differences in the L32 banding pattern (Fig. 1), expected large variations in densitometric data between corresponding pairs of autoradiographs were found
Summary
Studies from our laboratory have shown that human alveolar macrophages (AM) and bronchial epithelial cells (HBEC) exposed to ambient particles (PM10) in vitro increase their production of inflammatory mediators and that supernatants from PM10-exposed cells shorten the transit time of monocytes through the bone marrow and promote their release into the circulation. When AM and airway epithelial cells are directly exposed to inhaled atmospheric particles these small particles are phagocytized by both cells [10,12] Both cell types can synthesize a variety of pro-inflammatory cytokines that induce airway inflammation and contribute to the airway lesions in asthma and chronic obstructive pulmonary diseases [9]. Studies from our laboratory have shown that the PM10(EHC-93)-induced interaction of human AM and bronchial epithelial cells (HBEC) enhances the synthesis and release of a variety of proinflammatory cytokines and that supernatants from these co-cultures instilled into rabbit lungs induces a systemic inflammatory response [13]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
