Macrophages in asthma: 3 different types, 2 bad choices, 1 solution

Christina Draijer

Research output: ThesisThesis fully internal (DIV)

1043 Downloads (Pure)


Macrophages are immune cells that are abundantly present in the lung, though their contribution to asthma development and progression is unclear. Macrophages have diverse functions in the lung and they can easily change phenotype to accommodate these many functions. The three main phenotypes are pro-inflammatory M1, pro-repair M2 and anti-inflammatory M2-like. In this project we aimed to investigate how these macrophage subsets contribute to the development and progression of asthma.
We found that asthma in humans and experimental asthma in mice is characterized by higher numbers of M1 and M2 macrophages and lower numbers of M2-like macrophages. Tracing studies taught us that these higher numbers of M1 and M2 develop locally from proliferating alveolar macrophages and phenotype switching of interstitial macrophages. When we inhibited the development of M2 macrophages in experimental asthma we found the eosinophilic inflammation and remodeling of airways were inhibited but were replaced by neutrophilic inflammation with higher numbers of M1 macrophages and more airway hyperresponsivess. Induction of M2-like macrophages by treating with PGE2 was more promising as a therapeutic strategy because this inhibited overall inflammation. Interestingly, in asthma patients who used corticosteroids we also found higher numbers of M2-like macrophages, which correlated with less M1 macrophages being present. Therefore new treatment options may want to focus on the induction of the protective M2-like macrophages in asthma, especially for those patients that do not respond to corticosteroid treatment.
Original languageEnglish
QualificationDoctor of Philosophy
Awarding Institution
  • University of Groningen
  • Melgert, Barbro, Supervisor
  • Poelstra, Klaas, Supervisor
  • Hylkema, Machteld, Co-supervisor
Award date29-Apr-2016
Place of Publication[Groningen]
Print ISBNs978-90-367-8743-7
Electronic ISBNs978-90-367-8742-0
Publication statusPublished - 2016

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