Marcos López Hoyos
Scientific Director of the Valdecilla Health Research Institute (IDIVAL) and Professor of Immunology at the University of Cantabria
I love the work. It is a very well-targeted and well-managed work. It uses a very good number of volunteers: 1,000 volunteers with 200 per decade (100 and 100 per gender). They collect samples and a number of more than 100 socio-demographic and environmental variables.
I am convinced that more work will come out of this study, as there will be more results due to the methodology used.
It helps to explain possible alterations in the immune response that we frequently see in the clinic of smokers (and usually overweight) who reach the age of 60 with suspected immunodeficiency secondary to smoking in the context of chronic obstructive pulmonary disease (COPD) and where hypogammaglobulinemia [low antibody concentration] is seen relatively frequently.
The work provides data on inflammation due to activation of both the adaptive and innate immune responses, which contribute to complicating the course of COPD.
They relate the variables collected to data on the production of immune response cytokines produced in the supernatant of whole blood from volunteers subjected to different stimuli by microorganisms and by non-specific polyclonal stimuli, which is more consistent and biologically plausible, unlike many studies where cytokines are studied in serum, where we know there is a lot of variability.
The limitations are well identified by the authors, in particular the need for a validation cohort. From this study, validations will almost certainly be proposed.
In short, this is a very interesting study with clear clinical implications in a prevalent problem such as COPD, which presents with exacerbations and repeated infections that often lead to the suspicion of an immunological disorder. As the study indicates, smoking itself alters the immune response, and this has been very elegantly demonstrated.