Association of lower airway inflammation with physiologic findings in young children with cystic fibrosis

http://www.ncbi.nlm.nih.gov/pubmed/19382221?dopt=Abstract


take special note of the mention of neutrophils.... and if you need a refresher as to why this is important, visit the NAC studies on my blog :)

Mechanisms of the noxious inflammatory cycle in cystic fibrosis

Mechanisms of the noxious inflammatory cycle in cystic fibrosis http://snipurl.com/e0obk

Multiple evidences indicate that inflammation is an event occurring prior to infection in patients with cystic fibrosis. The self-perpetuating inflammatory cycle may play a pathogenic part in this disease. The role of the NF-kappaB pathway in enhanced production of inflammatory mediators is well documented.

The pathophysiologic mechanisms through which the intrinsic inflammatory response develops remain unclear. The unfolded mutated protein cystic fibrosis transmembrane conductance regulator (CFTRdeltaF508), accounting for this pathology, is retained in the endoplasmic reticulum (ER), induces a stress, and modifies calcium homeostasis.

Furthermore. CFTR is implicated in the transport of glutathione, the major antioxidant element in cells. CFTR mutations can alter redox homeostasis and induce an oxidative stress. The disturbance of the redox balance may evoke NF-kappaB activation and, in addition, promote apoptosis. In this review, we examine the hypotheses of the integrated pathogenic processes leading to the intrinsic inflammatory response in cystic fibrosis.


Glutathione - our good friend. Make sure to check out my NAC posts

Immune cells play surprising role in cystic fibrosis lung damage, Stanford/Packard study shows

http://snipurl.com/dydgo


5 points to anyone who knows what the answer is to excess neutrophils....


You guessed it! NAC!