The immune response against a bacterial aggression involves the monocytes-macrophages and polymorphonuclear neutrophils (PMN) in the first line of defense. This natural or innate immunity controls the proliferation of micro-organisms while waiting for the development of aspecific immunity related to lymphocytes. Establishing a link between innate and specific immunity, interleukin-12 (IL-12) is an essential cytokine of the inflammatory response. In a first in vitro study, we showed that IL-12 potentiates the effect of LPS on the production of IL-8 by stimulated PMN, the main chemotactic and activating cytokine of neutrophils. IL-12 would thus support the local recruitment of PMN via an autocrine loop of amplification. In a second in vivo study in septic patients, we noted a defect in the pulmonary and systemic production of IL-12, suggesting a dysregulation of innate immunity during the course of sepsis.