Figure 1.

Dynamic Clinical Immune Response to Infection. Dynamic Clinical Immune Response to Infection and Potential Sargramostim Effect. After transmission, an infectious pathogen incubates, replicates , and induces systemic inflammation . A high pathogen load can overwhelm and dysregulate the innate and adaptive immune systems, spread, and cause life-threatening organ dysfunction. An overly pro-inflammatory immune response leads to systemic inflammatory response syndrome (SIRS).The compensatory anti-inflammatory response syndrome (CARS) slows the immune response. Simultaneous SIRS and CARS are considered normal complementary physiologic mechanisms that balance to restore homeostasis after infection onset. However, complications or dysregulated immune systems can incite excessive SIRS or CARS, skew the balance, and induce damage to vital organs (e.g., lungs, kidneys, heart, GI system, brain) and cause multiple organ dysfunction syndrome (MODS), and death. In the case of respiratory viral infections, damage to the lungs can result in acute respiratory distress syndrome (ARDS). Sargramostim (recombinant human granulocytemacrophage colony-stimulating factor) may mirror the effects of endogenous GM-CSF to modulate the immune response by alveolar macrophage activation, dendritic cell maturation, and antigen-specific T cell recruitment to aid in pathogen clearance. This may mitigate hyperinflammation and immunoparalysis to prevent ARDS and other organ damage.