Journal
ANNUAL REVIEW OF PHYSIOLOGY
Volume 72, Issue -, Pages 413-435Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev-physiol-021909-135909
Keywords
innate immunity; antimicrobial; microbial killing; pneumonia
Categories
Funding
- NIH [RR02419, AI061555, U54 AI057156, HL72984, HL094848, AI82226]
- Texas A&M Health Science Center
- Hamill Foundation
- Cystic Fibrosis Foundation [08G0]
- George and Barbara Bush Endowment for Innovative Cancer Research
- NATIONAL CANCER INSTITUTE [P30CA016086] Funding Source: NIH RePORTER
- NATIONAL CENTER FOR RESEARCH RESOURCES [S10RR002419] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL072984, R21HL094848] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [U01AI082226, U54AI057156, R21AI061555] Funding Source: NIH RePORTER
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Most studies of innate immunity have focused on leukocytes such as neutrophils, macrophages, and natural killer cells. However, epithelial cells play key roles in innate defenses that include providing a mechanical barrier to microbial entry, signaling to leukocytes, and directly killing pathogens. Importantly, all these defenses are highly inducible in response to the sensing of microbial and host products. In healthy lungs, the level of innate immune epithelial function is low at baseline. This is indicated by low levels of spontaneous microbial killing and cytokine release, reflecting low constitutive stimulation in the nearly sterile lower respiratory tract when mucociliary clearance mechanisms are functioning effectively. This contrasts with the colon, where bacteria are continuously present and epithelial cells are constitutively activated. Although the surface area of the lungs presents a large target for microbial invasion, activated lung epithelial cells that are closely apposed to deposited pathogens are ideally positioned for microbial killing.
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