Welcome Dr. Bethany Moore to our Associate Editor team

Dear members of the lung community:

We are delighted to announce the appointment of Dr. Bethany Moore as Associate Editor of the American Journal of Physiology-Lung Cellular and Molecular Physiology, effective July 1^st. 

Bethany B. Moore graduated from the University of Texas at Austin with a degree in Microbiology in 1986.  She completed her Ph.D. in Immunology at the University of Texas Southwestern Medical Center in 1992.  She did post-doctoral training at U.T. Southwestern and Stanford in the field of molecular immunology before joining the faculty at the University of Michigan in 1997. She rose through the ranks and currently holds the position of full professor with tenure in the Departments of Internal Medicine and Microbiology and Immunology.  Dr. Moore’s research has focused on two main areas.  The first is the pathogenesis of pulmonary fibrosis and the second is in infectious complications in the lung following stem cell transplantation.  In her pulmonary fibrosis work, Dr. Moore has made contributions to our understanding of chemokine and eicosanoid regulation of the disease pathogenesis with a particular focus on alveolar-epithelial cell interactions and fibrocytes.  She has also studied how herpesviral infections, aging and matricellular proteins impact fibrotic disease outcomes.  Her work in these areas involves animal modeling as well as translational projects.  Her work in the area of stem cell transplantation has focused on alterations in innate immune cell function which increase susceptibility to bacterial infections and on alterations to adaptive immunity which impair host defense against viral pathogens.  She has demonstrated a major role for prostaglandin E₂ as an inhibitor of alveolar macrophage and neutrophil function post-transplant and is currently working to understand how effector T cell responses are skewed from protective Th1 to pathogenic Th17 responses leading to pneumonitis and fibrosis following herpesviral infection in transplant recipients.  She was the recipient of the Recognition Award for Scientific Accomplishment from the American Thoracic Society in 2014.  In addition to her research efforts, she directs the Graduate Program in Immunology at the University of Michigan. 
 

Mitochondrial DNA damage and repair: Role in acute lung injury

Mitochondrial DNA (mtDNA) contains 37 genes that encode 13 proteins, 22 tRNAs, and 2 rRNAs, which are involved in the synthesis of enzymes required for oxidative phosphorylation. Mitochondrial DNA is highly sensitive to oxidative damage (1), and studies have shown an association between mtDNA damage and oxidant-induced cell death (2). In a recent article in press (3) titled “Mitochondrial DNA damage-associated molecular patterns mediate a feed-forward cycle of bacteria-induced vascular injury in perfused rat lungs” in AJP-Lung Cellular and Molecular Physiology, Dr. Mark Gillespie and his team found interesting data that demonstrated that pulmonary exposure to bacteria, such as Pseudomonas aeruginosa, leads to oxidative mtDNA damage and the accumulation of mtDNA damage-associated molecular patterns (mtDNA DAMPs). These mtDNA DAMPs caused further damage to mtDNA integrity, increased vascular permeability, and propagated bacteria-induced lung injury. The study concluded by showing that the administration of a fusion protein that targets the DNA repair enzyme, Ogg1, blocked the deleterious effects of P. aeruginosa. This study was particularly interesting because it suggested that during infection, a feed-forward cycle of mtDNA DAMP formation and mtDNA damage culminates in acute lung injury. The clinical implications of this study are enormous, and it raises some interesting questions about the long-term management of patients with respiratory bacterial infections. Therefore, it may be possible to supplement antibiotics with agents that repair lung mtDNA to prevent the development of acute lung injury and acute respiratory distress syndrome. However, what still remains unanswered is the cell-type that mainly contributes to the formation of the mtDNA DAMPs, whether the DAMPs from one cell-type are equally damaging compared to the DAMPs from another cell-type, and if the repair of mtDNA of non-resident inflammatory cells would exacerbate the disease outcome and progression. These questions need to be furthered explored and would be of great interest.

Author: Dr. Saurabh Aggarwal MD. Ph.D., Instructor, Department of Anesthesiology, University of Alabama at Birmingham, AL

1. Grishko, V., Solomon, M., Wilson, G. L., LeDoux, S. P., and Gillespie, M. N. (2001) Am J Physiol Lung Cell Mol Physiol 280, L1300-1308
2. Grishko, V., Solomon, M., Breit, J. F., Killilea, D. W., Ledoux, S. P., Wilson, G. L., and Gillespie, M. N. (2001) FASEB J 15, 1267-1269
3. Kuck, J. L., Obiako, B. O., Gorodnya, O. M., Pastukh, V. M., Kua, J., Simmons, J. D., and Gillespie, M. N. (2015) Am J Physiol Lung Cell Mol Physiol, ajplung 00015 02015

How to publish your paper in AJP-Lung

AJP-Lung Star Reviewers

AJP-Lung would like to recognize our “Star Reviewers” for 2015 who were announced at the publications dinner at EB 2015. Congratulations to: Namasivayam Ambalavanan MD, Caroline Owen MD PhD and Christopher Waters PhD. Together they reviewed 38 submissions in 2015 with a average turnaround time of 8.3 days. Thank you very much for your dedication to AJP-Lung!

AJP-Lung plans for a new Associate Editor

The American Journal of Physiology-Lung Cellular and Molecular Physiology is now recruiting for an additional Associate Editor in the field of mitochondrial injury and repair to join our team of outstanding associate editors effective July 1st, 2015. Candidates should have an international reputation in the above fields, and will have been publishing in AJP-Lung during the last three years. Please send your CV along with a letter describing how your contribution will improve the impact of AJP-Lung in the lung community to the Editor in Chief(sadis@uab.edu) with a copy to the Editorial Assistant (Amy McEver, amcever@emory.edu). Refer to PMID: 25381028 for our editorial philosophy, accomplishments during the last three years and future challenges. The deadline for receipt of applications is June 1, 2015. Thank you!