Targeting the phosphoinositide-3-kinase/protein kinase B pathway in airway innate immunity

Figure 3 Summarization of non-specific immune strategies in lung innate immunity. Toll-like receptors are activated to recognize pathogen-associated microbial patterns/damage-associated molecular pattern (PAMPs/DAMPs) and activate nuclear factor-kB to produce cytokines; nod-like receptors are cytosolic receptors that can recognize intracellular PAMPs/DAMPs and can form inflammasome to either produce cytokines such as interferons or induce pyroptosis (inflammation associated apoptosis); Stimulation of bitter receptors, expressed in ciliated cells in the airways, elevates Ca²⁺ that produces NO which activates protein kinase G and increase ciliary beat frequency; NO can directly kill bacteria; Goblet cells produce mucus that traps pathogens and bacteria which are then eliminated out of the upper airway system through MCC; Activation of bitter receptors in solitary chemosensory cells can increase intracellular Ca²⁺ that can produce antimicrobial peptides.