In vivo T-cell activation by a monoclonal αCD3ε antibody induces preterm labor and birth.

PROBLEM: Activated/effector T cells seem to play a role in the pathological inflammation associated with preterm labor. The aim of this study was to determine whether in vivo T-cell activation by a monoclonal αCD3ε antibody induces preterm labor and birth. METHOD OF STUDY: Pregnant B6 mice were intraperitoneally injected with a monoclonal αCD3ε antibody or its isotype control. The gestational age, the rates of preterm birth and pup mortality at birth as well as the fetal heart rate and umbilical artery pulsatility index were determined. RESULTS: Injection of a monoclonal αCD3ε antibody led to preterm labor/birth (αCD3ε 83 ± 16.97% [10/12] vs isotype 0% [0/8]) and increased the rate of pup mortality at birth (αCD3ε 87.30 ± 8.95% [77/85] vs isotype 4.91 ± 4.34% [3/59]). In addition, injection of a monoclonal αCD3ε antibody decreased the fetal heart rate and increased the umbilical artery pulsatility index when compared to the isotype control. CONCLUSION: In vivo T-cell activation by a monoclonal αCD3ε antibody in late gestation induces preterm labor and birth.

Molecular mechanisms of reactive oxygen species-related pulmonary inflammation and asthma.

Asthma is a highly relevant disorder that can be induced by many environmental factors such as allergens and pollutants. One of the most critical pathological symptoms of asthma is airway inflammation. In order to identify a cause of respiratory inflammation, we thoroughly examine the unique role of reactive oxygen species (ROS). Evidence supports that the inhalation of aggravating compounds such as allergens can promote the increased generation of ROS. Accordingly, ROS have a proven role in the cellular signaling cascades of many respiratory diseases that cause respiratory inflammation, including asthma. Although there is no known cure for asthma, current treatments effectively lessen the inflammation symptom. Based on the investigations of asthma pathogenesis and the mechanism of ROS formation, we have identified several novel anti-inflammatory therapeutic treatments, shedding light on a fundamental understanding for the cure of this disorder. In this review, we will outline the pathogenesis of asthma and its relationship to ROS, oxidative stress, and pulmonary inflammation.