Inhaled insulin does not trigger lung inflammation and airway remodelling
To the Editors:
We read with great interest the paper by Liu et al. 1, regarding the effects of inhaled insulin on airway lining fluid composition in adults with diabetes. The study concluded that treatment with inhaled human insulin (Exubera®) is not associated with evidence of pulmonary inflammation and therefore the treatment effects on lung function observed in Exubera® trials are not caused by lung inflammation.
Local inflammation results in airway remodelling mediated by cytokines produced by recruited inflammatory cells, as well as by airway myofibroblasts and airway smooth muscle (ASM) cells 2. ASM cells maintain their plasticity exhibiting a differentiated contractile or a synthetic proliferative phenotype in response to physiological and pathological signals 3. In a relevant study, we examined the possibility that growth-promoting properties of inhaled insulin play a role in airway remodelling 4. Our findings regarding insulin's effect on rabbit tracheal ASM cell proliferation, show that insulin transiently promotes cell proliferation in ASM cells by the activation of the phosphoinositide 3-kinases. Importantly, longer incubation with insulin didn't lead to additional cell growth.
Therefore, the in vivo study by Liu et al. 1 together with our in vitro study 4 suggest that long-term exposure of the airways to insulin, as in the administration of inhaled insulin in patients with diabetes mellitus, is not likely a risk factor for inflammation and airway remodelling.
Statement of interest
None declared.
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