Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interleukin (IL)-27 is a unique cytokine that has a dual role in immune responses. It was originally described to promote Th1 differentiation but also suppresses inflammation by inhibiting these and other inflammatory T cell subsets. Inhibition of inflammatory activity in macrophages has also been reported. These reports have largely focused on cytokine profiles or signaling mechanisms. To date, there have been no reports of how IL-27 may directly influence cellular mechanisms that operate to control microbial growth. Formation of a phagolysosome that acquires antimicrobial properties is an essential step for destruction of pathogens or pathogen-derived materials that are internalized by macrophages. Here we report that IL-27 has a profound influence on this critical innate immunity pathway. Treatment of human macrophages with IL-27 interferes with the acidification of phagosomes by reducing protein levels of V-ATPase and impairs control of bacterial pathogens.
Cytokine 2013 May
PMID:Interleukin-27 inhibits phagosomal acidification by blocking vacuolar ATPases. 2355 95

Acute lung injury leading to acute respiratory distress (ARDS) is a global health concern. ARDS patients have significant pulmonary inflammation leading to flooding of the pulmonary alveoli. This prevents normal gas exchange with consequent hypoxemia and causes mortality. A thin fluid layer in the alveoli is normal. The maintenance of this thin layer results from fluid movement out of the pulmonary capillaries into the alveolar interstitium driven by vascular hydrostatic pressure and then through alveolar tight junctions. This is then balanced by fluid reabsorption from the alveolar space mediated by transepithelial salt and water transport through alveolar cells. Reabsorption is a two-step process: first, sodium enters via sodium-permeable channels in the apical membranes of alveolar type 1 and 2 cells followed by active extrusion of sodium into the interstitium by the basolateral Na+, K+-ATPase. Anions follow the cationic charge gradient and water follows the salt-induced osmotic gradient. The proximate cause of alveolar flooding is the result of a failure to reabsorb sufficient salt and water or a failure of the tight junctions to prevent excessive movement of fluid from the interstitium to alveolar lumen. Cytokine- and chemokine-induced inflammation can have a particularly profound effect on lung sodium transport since they can alter both ion channel and barrier function. Cytokines and chemokines affect alveolar amiloride-sensitive epithelial sodium channels (ENaCs), which play a crucial role in sodium transport and fluid reabsorption in the lung. This review discusses the regulation of ENaC via local and systemic cytokines during inflammatory disease and the effect on lung fluid balance.
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PMID:Regulation of Lung Epithelial Sodium Channels by Cytokines and Chemokines. 2879 Oct 6


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