Neutrophils play an important role in the host defense by invading microbial pathogens. Upon infection neutrophils become activated through interaction with chemo attractants and cytokines. These ligands bind to a variety of cell surface receptors, including heterotrimeric GPCR (G-Protein Coupled Receptors) for fMLP (N-formyl-Met-Leu-Phe) and PAF (Platelet Activating Factor), and tyrosine kinase-associated receptors for GMCSF (Granulocyte-Macrophage Colony Stimulating Factor). Receptor activation triggers intracellular signal transduction pathways, resulting in the correct biological response, for instance, migration, phagocytosis, antibody-dependent cell mediated cytotoxicity, degranulation, superoxide production, transcriptional activation, and actin reorganization. If G-protein is blocked by pertussis toxin, cells do not respond to fMLP (Ref.1). Improper functioning of neutrophils is implicated in the pathogenesis of a variety of inflammatory diseases resulting in tissue damage (Ref.2). [...]