Abstract
Inflammation is a key component of asthma. Membrane-bound chemokine CX3CL1 is markedly induced on endothelial cells by inflammatory cytokines, and CX3CL1 levels are elevated in the bronchoalveolar lavage (BAL) of subjects with asthma. Recently, CX3CR1 (the receptor for CX3CL1) has been proposed as a target for airway inflammation, and the paper proposing this was evaluated. The paper established a link between CX3CR1 and asthma, as reducing the availability of CX3CR1, or inhibiting the responses mediated by the CX3CR1, resulted in reduced asthma in a mouse model. This suggests that agents blocking the CX3CR1 may be useful in the treatment of asthma. However, there are reports suggesting that glucocorticoids may downregulate the CX3CL1–CX3CR1 pathway in inflammation. Thus, the next step is to establish whether inhibitors of the CX3CL1–CX3CR1 pathway have any additional, or different, effects to glucocorticoids, in the treatment of airway inflammatory disorders, in animal models. Subsequently, further consideration can be given to the development of CX3CR1 as a target for airway inflammation in humans.
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