Cs exposure increased apoptosis and emphysematous

IL-6 cytokine family that signals through a common gp130 coreceptor associated with the pathogenesis of emphysema. However, the final

mechanisms by which these cytokines cause emphysema remain unclear. We have

in vivo genetic approach to determine the addition of specific IL-6 family of cytokines and gp130 regulated cellular processes

, that causes emphysema. We used

gp130 mice lasix buy homozygous for a subtle knock in mutations in gp130, which deregulates intracellular signaling in IL-6 cytokine family.

Gp130 mice spontaneously develop emphysema at the age of 6 months. In IL-6 cytokine family, only IL-6 was much more regulated in easily

gp130 mice and genetic targeting of IL-6 in mice

gp130 (gp130: IL -6) to prevent emphysema. In contrast, genetic removal of receptor signaling by IL-11, which, like IL-6 signals through gp130

homodimer and uses the same mechanism of signaling could improve emphysema in

gp130 mice. Among the diseases related processes considered, emphysema correlates with increased apoptosis of alveolar cells. Acute (4 days), the effect of cigarette smoke (CS) further added to the expression of IL-6 in easily

gp130 mice and subacute (6 weeks) CS exposure increased apoptosis and emphysematous changes in lung

gp130, but not gp130: IL-6 in mice. IL-6 is the major causative agent of IL-6 cytokine family caused by emphysema, and works to cause apoptosis in the lungs >>. << We believe that discrete attack on IL-6 signaling may provide an effective therapeutic strategy against human lung diseases >>. <<.