Toll-like receptor expression in severe asthma with chronic rhinosinusitis

Background We have in an epidemiological study identified a group of individuals with multiple asthma symptoms (MSA) that reflect a more severe and uncontrolled disease. An altered innate immunity and adaptive immunity, and effects of microorganisms may play a role in the development of both CRS and asthma. The innate immune system use Toll-like receptors (TLRs) to recognize microbes and activate defense mechanisms within minutes of microbial invasion which is followed by an antigen-specific response by the adaptive immune system. Thus, innate and adaptive immune cells are sequentially activated and reciprocally regulate one another. Glycogen synthase kinase-3b (GSK3b) has been demonstrated as a regulator of both innate and adaptive immunity. GSK3b was shown to modulate inflammatory responses through TLR-mediated production of pro-inflammatory cytokines and inactivation of GSK3b (phosphorylated GSK3b) lead to a reduced IL-12 production, which was suggested to skew the balance towards a Th2 response.