Emergent evidence indicates that the carotid body (CB) chemoreceptors may sense systemic inflammatory molecules, and is an afferent-arm of the anti-inflammatory reflex. Moreover, a pro-inflammatory milieu within the CB is involved in the enhanced CB chemosensory responsiveness to oxygen following sustained and intermittent hypoxia. In this review, we focus on the physio-pathological participation of CBs in inflammatory diseases, such as sepsis and intermittent hypoxia.