Injury to the lung when viewed on histopathology, nor is there a significant increase in cells recruited to the alveoli when measured in bronchoalveolar lavage fluid at 24 hours. The in vitro macrophage data suggests the administered agmatine may have stimulated the resident cells of the lung without inducing a measurable recruitment of neutrophils. In an attempt to replicate the co-stimulatory conditions of the cell culture experiments we intratracheally injected both LPS and agmatine into the lungs of mice. However the inflammatory response over the lungs alone was difficult to measure given the robust systemic response to LPS in the liver and abdomen. Using a similar NF-kB reporter mouse we administered both LPS and agmatine via the intraperitoneal route and measured the total body NF-kB response in this model. At 4 hours agmatine augments the LPS induced NF-kB response, but this response is more rapidly diminished by 8 hours. As with the cellular response, the systemic response to agmatine and LPS in an animal model is likely complex, however it is clear that agmatine administration does augment the inflammatory response in vitro and in vivo when exogenously administered. With advances in analytical techniques, the ability to track multiple small molecules in diverse matrices has led to a heightened appreciation of the complicated chemical mediators of both immune cell and bacterial signaling. Frequently these signaling molecules, such as cytokines and quorum sensing molecules, are unique to a species, having the presumed intent of communicating a very specific message to neighboring cells. Occasionally a pathogen may adapt a way to intercept or destroy cell signaling molecules with potential benefit to bacterial survival. This work on the arginine decarboxylase pathways of mammals and bacteria was spawned by the observation that the benign molecule agmatine induces select P. aeruginosa strains to form a biofilm. Agmatine has no deleterious effect on P. aeruginosa up to millimolar quantities, and is readily metabolized to putrescine which can be a source of ATP production after conversion to alanine or succinate. While many of the cues that coerce a pathogen to form a biofilm are not known, most are thought to be cues of environmental stress. This suggests that agmatine may be a cue of stress to P. aeruginosa in one of its natural environments. Agmatine has not been described in the human lung until now. Its role in human biology is poorly understood having only recently been shown to exist in mammals. It has known receptor affinities for a2-adrenoreceptors, serotonin, and SB203580 imidazoline receptors, and has been shown to be a direct inhibitor to NOS-2 presumably given its similarity to the NOS substrate arginine. It is not known how important agmatine is in most organ systems, or if its receptor actions are evolutionarily intended or merely a consequence of similarity to the known ligands of each of those receptors.