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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Front+Cell+Infect+Microbiol
2020 ; 10
(ä): 300
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Participation of the IL-10RB Related Cytokines, IL-22 and IFN-? in Defense of the
Airway Mucosal Barrier
#MMPMID32637365
Ahn D
; Prince A
Front Cell Infect Microbiol
2020[]; 10
(ä): 300
PMID32637365
show ga
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-? (IFN-?), 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-?, 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.