Abstract
Detailed analysis of the effects of ICS on parameters beyond inflammation and lung function in COPD are needed http://ow.ly/mPN530c035q
From the authors:
We thank Dr Sohal and his colleagues for their correspondence regarding our recently published article in the European Respiratory Journal (ERJ) about airway inflammation in chronic obstructive pulmonary disease (COPD) after withdrawal of inhaled corticosteroids (ICS) [1]. We agree that COPD includes much more than airflow obstruction and airway inflammation alone and we would like to briefly respond to the issues raised in the correspondence.
The observation by Sohal et al. [2] that total airway wall cellularity is lower in smokers and COPD patients is interesting. In the GLUCOLD (Groningen and Leiden Universities Corticosteroids in Obstructive Lung Disease) study, we focused only on COPD patients and on changes in mucosal cell numbers for specific subsets of inflammatory and immune cells. Therefore, we cannot link our data to their conclusion on decreased cellularity in COPD. Sohal and colleagues also note that we detected higher numbers of CD4+ T-cells than CD8+ T-cells and that this is in contrast to their findings. We have noted this difference in previous studies [3], as have other study groups [4–6] who have also described higher numbers of CD4 cells than CD8 cells in COPD. Furthermore, our data show good internal consistency during the various time points, which strengthens our results. It should be noted, however, that other studies have reported similar numbers of CD8 and CD4 cells [7, 8] while still more (including Sohal and colleagues) report higher numbers of CD8 cells than CD4 cells in the airway wall tissue of COPD patients [9, 10]. These differences in the CD4/CD8 ratio in airway walls are therefore important to note and are likely to represent phenotypic heterogeneity amongst patients with COPD. It should be noted, however, that we cannot exclude an influence due to differences in immunohistochemical technique between these studies (such as the monoclonal antibodies used to quantify cell numbers). Sohal and colleagues also raise interesting and important questions regarding epithelial mesenchymal transition (EMT), vascularity and basal cell reprogramming in COPD. These are indeed important features of COPD that might be influenced by corticosteroid treatment. It is unfortunate that we do not have any data regarding these parameters.
We fully agree with Sohal and colleagues that collaboration between various centers is needed to address important issues regarding the pathology of COPD and its relationship to lung function and treatment response. This is indeed one of the reasons why the GLUCOLD study not only involves collaboration between various departments amongst the university medical centers of Groningen and Leiden in the Netherlands, but also includes contributions from other centers such as the pathology group of Thais Mauad at the University of São Paulo in Brazil. Indeed, larger international networks using standardised methodology are essential to shed further light on this important aspect of COPD research.
Disclosures
Supplementary Material
P.S. Hiemstra ERJ-00848-2017_Hiemstra
H.A.M. Kerstjens ERJ-00848-2017_Kerstjens
L.I.Z. Kunz ERJ-00848-2017_Kunz
D.S. Postma ERJ-00848-2017_Postma
J.K. Sont ERJ-00848-2017_Sont
P.J.Sterk ERJ-00848-2017_Sterk
W. Timens ERJ-00848-2017_Timens
Acknowledements
The GLUCOLD study group consists of the following participants. H.F. Kauffman and D. de Reus (Dept of Allergology); H.M. Boezen, D.F. Jansen and J.M. Vonk (Dept of Epidemiology); M.D.W. Barentsen, W. Timens and M. Zeinstra-Smit (Dept of Pathology); A.J. Luteijn, T. van der Molen and G. ter Veen (Dept of General Practice); M.M.E. Gosman, N.H.T. ten Hacken, H.A.M. Kerstjens, M.S. van Maaren, D.S. Postma, C.A. Veltman, A. Verbokkem, I. Verhage and K. Klooster (Dept of Pulmonology; all University of Groningen and University Medical Center Groningen, Groningen, the Netherlands). H.A. Thiadens (Dept of General Practice); J.B. Snoeck-Stroband and J.K. Sont (Dept of Medical Decision Making); J. Gast-Strookman, P.S. Hiemstra, K. Janssen, K.F. Rabe, A. van Schadewijk, J.A. Schrumpf, J. Smit-Bakker, J. Stolk, A.C.J.A. Tiré, H. van der Veen, M.M.E. Wijffels and L.N.A. Willems (Dept of Pulmonology; all Leiden University Medical Center, Leiden, the Netherlands). P.J. Sterk (Dept of Respiratory Medicine, Academic Medical Centre, University of Amsterdam, Amsterdam, the Netherlands). T.S. Lapperre (Dept of Respiratory and Critical Care Medicine, Singapore General Hospital, Singapore, Singapore). T. Mauad (University of São Paulo, São Paulo, Brazil).
Footnotes
Conflict of interest: Disclosures can be found alongside this article at erj.ersjournals.com
- Received April 23, 2017.
- Accepted May 4, 2017.
- Copyright ©ERS 2017