The airway epithelial barrier is a major barrier protecting against clinically significant infections of the lung. Its integrity is often compromised due to mechanical, chemical, or infectious causes. Opportunistic bacterial pathogens are poised to cause parenchymal infection and become difficult to eradicate due to adaptive metabolic changes, biofilm formation, and the acquisition of antimicrobial resistance and fitness genes. Enhancing mucosal defenses by modulating the cytokines that regulate barrier functions, such as interleukin-22 (IL-22) and interferon-λ (IFN-λ), members of the IL-10 family of cytokines, is an attractive approach to prevent these infections that are associated with high morbidity and mortality. These cytokines both signal through the cognate receptor IL-10RB, have related protein structures and common downstream signaling suggesting shared roles in host respiratory defense. They are typically co-expressed in multiple models of infections, but with differing kinetics. IL-22 has an important role in the producing antimicrobial peptides, upregulating expression of junctional proteins in the airway epithelium and working in concert with other inflammatory cytokines such as IL-17. Conversely, IFN-λ, a potent antiviral in influenza infection with pro-inflammatory properties, appears to decrease junctional integrity allowing for bacterial and immune cell translocation. The effects of these cytokines are pleotropic, with pathogen and tissue specific consequences. Understanding how these cytokines work in the mucosal defenses of the respiratory system may suggest potential targets to prevent invasive infections of the damaged lung.

气道上皮屏障是防止临床上重要的肺部感染的主要屏障。由于机械，化学或传染性原因，其完整性经常受到损害。由于适应性代谢变化，生物膜形成以及获得抗菌素耐药性和适应性基因，机会细菌性病原体随时可能引起实质性感染并难以根除。通过调节调节屏障功能的细胞因子（如IL-10细胞因子家族的成员白细胞介素22（IL-22）和干扰素-λ（IFN-λ））来增强粘膜防御能力，是预防此类感染的一种有吸引力的方法与高发病率和高死亡率有关。这些细胞因子都通过同源受体IL-10RB发出信号，具有相关的蛋白质结构和共同的下游信号传导，提示宿主呼吸防御中的共同作用。它们通常在多种感染模型中共表达，但动力学不同。IL-22在产生抗菌肽，上调气道上皮中连接蛋白的表达并与其他炎性细胞因子（如IL-17）协同作用中发挥重要作用。相反，IFN-λ是具有促炎特性的流感病毒感染中的一种有效抗病毒剂，它似乎会降低连接完整性，从而使细菌和免疫细胞易位。这些细胞因子的作用是多效的，具有病原体和组织特异性的后果。