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  • in the absence of endotoxins.[5-7] After inhalation, endotoxins, such as lipopolysaccharide (LPS), encounter and activate alveolar macrophages, leading to the production and release of pro-inflammatory cytokines, chemokines, adhesion molecules and other mediators.[8] Nasal and lung lavage samples of allergic subjects show increased levels of interleukin-1?? (IL-1??),[9] primarily produced by acti
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