Cigarette smoke increases TLR4 and modifies LPS mediated responses in airway epithelial cells.

Maria Rosaria Bonsignore, Angela M. Montalbano, Giovanni Bonsignore, Maria Ferraro, Malcolm Johnson, Mark Gjomarkaj, Mario Melis, Liboria Siena, Elisabetta Pace

Risultato della ricerca: Articlepeer review

137 Citazioni (Scopus)


Airway epithelium is emerging as a regulator of innate immune responsesto a variety of insults including cigarette smoke. The main goal of thisstudy was to explore the effects of cigarette smoke extracts (CSE) on Tolllikereceptor (TLR) expression and activation in a human bronchial epithelialcell line (16-HBE). The CSE increased the expression of TLR4 andthe lipopolysaccharide (LPS) binding, the nuclear factor-jB (NF-jB) activation,the release of interleukin-8 (IL-8) and the chemotactic activitytoward neutrophils. It did not induce TLR2 expression or extracellularsignal-regulated signal kinase 1/2 (ERK1/2) activation. The LPS increasedthe expression of TLR4 and induced both NF-jB and ERK1/2 activation.The combined exposure of 16-HBE to CSE and LPS was associated withERK activation rather than NF-jB activation and with a further increaseof IL-8 release and of chemotactic activity toward neutrophils. Furthermore,CSE decreased the constitutive interferon-inducible protein-10(IP-10) release and counteracted the effect of LPS in inducing both theIP-10 release and the chemotactic activity toward lymphocytes. In conclusion,cigarette smoke, by altering the expression and the activation ofTLR4 via the preferential release of IL-8, may contribute to the accumulationof neutrophils within the airways of smokers.
Lingua originaleEnglish
pagine (da-a)401-411
Numero di pagine11
Stato di pubblicazionePublished - 2008

All Science Journal Classification (ASJC) codes

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  • ???subjectarea.asjc.2400.2403???


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