6
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Bronchial inflammation and bacterial load in stable COPD is associated with TLR4 overexpression.

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Toll-like receptors (TLRs) and nucleotide-binding oligomerisation domain (NOD)-like receptors (NLRs) are two major forms of innate immune sensors but their role in the immunopathology of stable chronic obstructive pulmonary disease (COPD) is incompletely studied. Our objective here was to investigate TLR and NLR signalling pathways in the bronchial mucosa in stable COPD.Using immunohistochemistry, the expression levels of TLR2, TLR4, TLR9, NOD1, NOD2, CD14, myeloid differentiation primary response gene 88 (MyD88), Toll-interleukin-1 receptor domain-containing adaptor protein (TIRAP), and the interleukin-1 receptor-associated kinases phospho-IRAK1 and IRAK4 were measured in the bronchial mucosa of subjects with stable COPD of different severity (n=34), control smokers (n=12) and nonsmokers (n=12). The bronchial bacterial load of Pseudomonas aeruginosa, Haemophilus influenzae, Moraxella catarrhalis and Streptococcus pneumoniae was measured by quantitative real-time PCR.TLR4 and NOD1 expression was increased in the bronchial mucosa of patients with severe/very severe stable COPD compared with control subjects. TLR4 bronchial epithelial expression correlated positively with CD4(+) and CD8(+) cells and airflow obstruction. NOD1 expression correlated with CD8(+) cells. The bronchial load of P. aeruginosa was directly correlated, but H. influenzae inversely correlated, with the degree of airflow obstruction. Bacterial load did not correlate with inflammatory cells.Bronchial epithelial overexpression of TLR4 and NOD1 in severe/very severe stable COPD, associated with increased bronchial inflammation and P. aeruginosa bacterial load, may play a role in the pathogenesis of COPD.

          Related collections

          Author and article information

          Journal
          Eur. Respir. J.
          The European respiratory journal
          European Respiratory Society (ERS)
          1399-3003
          0903-1936
          May 2017
          : 49
          : 5
          Affiliations
          [1 ] Divisione di Pneumologia e Laboratorio di Citoimmunopatologia dell'Apparato Cardio Respiratorio, Istituti Clinici Scientifici Maugeri SpA, Società Benefit, Veruno, Italy antonino.distefano@icsmaugeri.it.
          [2 ] Dipartimento di Scienze Cliniche e Biologiche, AOU, San Luigi, Orbassano, Università di Torino, Turin, Italy.
          [3 ] Centro Interdipartimentale per lo Studio delle Malattie Infiammatorie delle Vie Aeree e Patologie Fumo-correlate (CEMICEF), Sezione di Medicina Interna e Cardiorespiratoria, Università di Ferrara, Ferrara, Italy.
          [4 ] Airways Disease Section, National Heart and Lung Institute, Imperial College London, London, UK.
          [5 ] Dipartimento di Medicina Molecolare, Università di Padova, Padua, Italy.
          [6 ] Dept of Neuroscience, Ophthalmology Unit, University of Padua, Padua, Italy.
          [7 ] UOC di Malattie Respiratorie, Dipartimento di Scienze Biomediche, Odontoiatriche e delle Immagini Morfologiche e Funzionali, Università di Messina, Messina, Italy.
          [8 ] Divisione di Pneumologia e Laboratorio di Citoimmunopatologia dell'Apparato Cardio Respiratorio, Istituti Clinici Scientifici Maugeri SpA, Società Benefit, Veruno, Italy.
          [9 ] Dipartimento di Oncologia, SCDU, Anatomia Patologica, AOU, San Luigi, Orbassano, Università di Torino, Turin, Italy.
          [10 ] Dipartimento di Biomedicina Sperimentale e Neuroscienze Cliniche, Sezione di Anatomia Umana, Università di Palermo, Palermo, Italy.
          [11 ] Euro-Mediterranean Institute of Science and Technology (IEMEST), Palermo, Italy.
          Article
          49/5/1602006
          10.1183/13993003.02006-2016
          28536249
          967c099e-fd06-4bbf-80ff-db5874a7e1f5
          History

          Comments

          Comment on this article