By contrast, in tobacco-related COPD, the activation of these pathways may be partly counterbalanced by neutrophil-related cytokines (e.g., IL-1β, IL-6, and IL-23), steering the response toward Th1/Th17 and thus limiting eosinophilic infiltration.30 Nevertheless, in patients with COPD secondary to smoking who do develop an eosinophilic endotype, it is reasonable to assume that the same alarmins orchestrate this response, influenced by factors such as infections or environmental pollution. Here, IL6 is linked to infection.