Ostepopontin (OPN) is a remarkable substance. The many aliases already point towards a multitude of biological functions: SPP1=secreted phosphoprotein 1, BSPI 1=bone sialoprotein-1, CIT, ETA-1, GC110940, nephropontin, osteoprotegerin, uropontin, bone sialoprotein I, early T-lymphocyte activation among others. Continue reading Osteopontin bridging air pollution and immunology of allergic inflammation
In a previous paper I have questioned if LPS
nanogram exposure on the pulmonary epithelium will supersede the gram-wise exposure on the gut mucosa.
This may indeed work as now shown by Eyal Raz in a commentary in Nature Immunology where previous TLR studies
typically reproduce the splenic version of innate immunity (the spleen is used here as a metaphor for the sterile internal environment).
In the lung only the alveolar space is thought to be sterile while macrophages should not be in a constant state of activation (as inflammation would compromise gas exchange).
There are now several indicators for a lung-specific regulation of innate immunity: TLR9 is expressed in human plasmacytoid dendritic cells while TLR4 is only on myeloid DCs; TGFB-ß mediated crosstalk between alveolar macrophages and epithelial cells seems to be unique in the lung; in addition indeolamine induction or surfactant production is not found elsewhere. Yea, yea.