Cobalt Chloride Can Induce a Respiratory Immune Response after Dermal Exposure in a Mouse Model

Cobalt is widely used in industries, and has been associated with occupational asthma and allergic contact dermatitis. However, the link between skin exposure and lung responses to cobalt is currently unknown. We have investigated this in a mouse model. On days 1 and 8, BALB/c mice were dermally treated (20µl/ear) with 5% CoCl2 or the vehicle dimethyl sulfoxide (DMSO). The mice received endotracheal challenges with 50 µl of 0.05% CoCl2 or saline on days 15, 17, 19, 22 and 24. In vivo micro-computed tomography (µCT) was performed on several timepoints. One day after the last challenge, we measured airway hyperreactivity to methacholine, lung inflammation in bronchoalveolar lavage (BAL), innate lymphoid cells (ILC) and dendritic cells (DC) in the lungs and serum immunoglobulins. All mice that received challenges with CoCl2 showed a significant increase in non-aerated lung volume on day 25, as assessed by µCT and a minor increase in neutrophils in BAL. Yet, only the CoCl2 dermally sensitized and CoCl2 challenged mice showed airway hyperreactivity to methacholine, a significant increase in eosinophils (7.2% vs. 0.2% in control group) along with the neutrophils (4.0% vs. 1.1%) in BAL, and a significantly higher number of total DCs (10.0% vs. 7.6%) and ILC2 (67.6% vs. 64.9%) in lung tissue. In conclusion, dermal sensitization, followed by multiple airway challenges with CoCl2 leads to a type 2 asthma-like immune response.