Interleukin-6 has no effect on surfactant or lung function in different lung insults.

The current study determined if interleukin-6 (IL-6) had a causative role in the lung dysfunction and/or surfactant alterations associated with three different lung insults. IL-6 (or saline) was instilled into rats followed by mechanical ventilation in vivo for 4 hours. Also, IL-6 (-/-) and wild-type mice were subjected to 3 insults: ex vivo injurious mechanical ventilation; cecal ligation and perforation; and hyperoxia exposure.

Differential response of TIMP-3 null mice to the lung insults of sepsis, mechanical ventilation, and hyperoxia.

An imbalance in matrix metalloproteinases (MMPs) and the tissue inhibitors of metalloproteinases (TIMPs) leads to excessive or insufficient tissue breakdown, which is associated with many disease processes. The TIMP-3 null mouse is a model of MMP/TIMP imbalance, which develops air space enlargement and decreased lung function. These mice responded differently to cecal ligation and perforation (CLP)-induced septic lung injury than wild-type controls.

Negative impact of tissue inhibitor of metalloproteinase-3 null mutation on lung structure and function in response to sepsis.

Matrix metalloproteinases (MMPs) are degradative enzymes, which act to remodel tissue. Their activity is regulated by the tissue inhibitors of metalloproteinases (TIMPs). An imbalance in the degradation/inhibition activities has been associated with many diseases, including sepsis.