Awards sponsored by the American Journal of Physiology-Lung Cellular and Molecular Physiology

The editors of the AJP-Lung and the APS are sponsoring a number of awards to recognize outstanding papers published in this journal.  They include one award for the Best Research Paper, three for the Hermann Rahn Award and two for the Usha Awards.  Please see the information in the APS webpage

http://www.the-aps.org/mm/awards/sections/Resp

 

We are looking forward to nominations and self-nominations. 

 

Sadis Matalon

Editor-in-Chief

APSselect features two AJP-Lung papers in August

APSselect is a collection of the very best original research papers published by the American Physiological Society.  Congratulations on our newest two APSselect winners for August.

Valeriy Poroyko and his colleagues for: 

Alterations of lung microbiota in a mouse model of LPS-induced lung injury. 
vol. 309: L76-L83, 2015. DOI: 10.1152/ajplung.00061.2014






and
Kelly S. Schweitzer et al, for their work:

Endothelial disruptive proinflammatory effects of nicotine and ecigarette vapor exposures.
vol. 309: L175-L187, 2015. DOI: 10.1152/ajplung.00411.2014

To view all the "best" papers that the American Physiology Society published in August  please visit http://apsselect.physiology.org/

Call for papers: Electronic cigarettes: not all good news?

Electronic cigarettes (e-cigs) are battery-operated devices which heat a liquid that contains nicotine, flavors, and additives and, in some cases, varying amounts of other unknown compounds, which are not regulated by the FDA. Aggressive advertising by e-cigs manufacturers implies these devices are less harmful and represent a “safe” alternative to conventional cigarette smoking. E-cigs reportedly contain less carcinogens than traditional cigarettes, with a predominance of nicotine in e-cig vapors that has led to them being variably called “nicotine delivery devices”. Thus, the assumption is that e-cigs cause less lung injury in the healthy user, and may help conventional cigarette users to quit smoking. Furthermore, e-cigs are viewed as being potentially safe for asthmatic smokers. Based on these purported safety profiles, e-cig use is increasing at an alarming rate.

In spite of the increasing use of e-cigs, data on their short- or long-term detrimental effects and toxicity are missing. In addition to the fact that the local heating and “vape” delivery by e-cigs has the potential to deliver substantially higher levels of nicotine to the upper and lower airways, e-cigs also contain formaldehyde, hemiacetals that can form formaldehyde, acrolein, and particulate matter, all of which can be potentially harmful. Furthermore, local delivery of e-cig products to the oropharynx and upper airways has the potential to substantially influence the oral and bronchial epithelium and salivary glands, thus influencing mucus membrane properties, barrier function, and immune responses and responsivity.  Indeed, salivary gland dysfunction can lead to periodontal disease, gingivitis, bacterial colonization, and loss of enamel mineralization.  These conditions are often encountered in conventional smokers and may be present in e-cig users as well. Similarly, higher nicotine or other product levels may adversely influence upper airway irritability, reflex bronchoconstriction and other key aspects of airway function. Finally, the influence of e-cig products on the alveolar epithelium and the pulmonary endothelium are still under exploration. In a recently article published in AJP-Lung and highlighted in a variety of electronic media,  Dr. Petrache and her collaborators demonstrated that nicotine and other components present in e-cigs damaged endothelial cells and increase endothelial permeability in addition to damaging airway and alveolar epithelia: http://ajplung.physiology.org/content/early/2015/05/11/ajplung.00411.2014. Clearly additional research is needed on this very interesting topic

The American Journal of Physiology-Lung Cellular and Molecular Physiology is issuing a call for papers addressing key questions in the mechanisms and potentially toxic effects of e-cigs as it applies to the cardiopulmonary system and other organs that may be targeted.  All manuscripts will be reviewed promptly, thoroughly, and fairly by members of the Editorial Board and guest reviewers who are recognized experts in this field. Accepted manuscripts will be published on line within two weeks after acceptance under a distinct heading and will receive special attention and handling. In addition, the Editor will solicit an annual perspective on this area to review seminal findings. Only those papers not requiring extensive revision will be published under this call for papers. 

This call for papers is effective between August 1^st, 2015 and October 1^st, 2017.

Mark N Gillespie, Ph.D. has joined the AJP-Lung team.

We are delighted to announce the appointment of Dr. Mark Gillespie as Associate Editor of the American Journal of Physiology-Lung Cellular and Molecular Physiology, his appointment was effective July 1, 2015.

Dr. Gillespie is a native of Chicago, IL, received his undergraduate and Ph.D. degrees from the University of Kentucky in 1977 and 1981, respectively.  He was a postdoctoral Fellow at the University of Colorado’s Cardiovascular-Pulmonary Research Laboratory until 1982 after which he was recruited back to the University of Kentucky where he rose to the rank of Professor and Chairperson of Pharmacology and Experimental Therapeutics.  In 1995, he relocated to his current affiliation, the University of South Alabama, where he serves as Professor and Chair of Pharmacology and founding member of the Center for Lung Biology.  Over the past two decades, Dr. Gillespie has served as ad hoc or regular member or chairperson of multiple NIH study sections and held leadership positions in organizations dedicated to lung health and disease.   His research program, supported continuously by the NIH and other agencies for the past 30 years, focuses on selected aspects of lung biology and pathology, most recently concentrating on how oxidative damage and repair in the nuclear and mitochondrial genomes dynamically regulates lung cell responses to oxidant stress.

Plasma gelsolin improves host defense

Plasma gelsolin improves lung host defense against pneumonia by enhancing macrophage NOS3 function

Zhiping Yang , Terry Ting-Yu Chiou , Thomas P. Stossel , Lester Kobzik

American Journal of Physiology - Lung Cellular and Molecular Physiology Published 1 July 2015 Vol. 309 no. 1, L11-L16 DOI: 10.1152/ajplung.00094.2015 

Bacterial pneumonia remains a leading cause of morbidity and mortality worldwide, and bacterial pneumonia occurring post-influenza infection is a devastating complication.  With the growing problem of antibiotic-resistant bacterial species, it is imperative for scientists to investigate ways to enhance the body’s own immune defense against potentially pathogenic microorganisms.  In terms of respiratory infections, the alveolar macrophage within the lung is the sentinel phagocyte responsible for patrolling airspaces and clearing pathogens.  In this issue of AJP Lung, Yang et al. describe the ability of a protein normally found in human blood called plasma gelsolin to enhance the ability of alveolar macrophages to kill ingested pathogens.  Plasma gelsolin has previously been shown to have beneficial functions for limiting inflammatory reactions, and it has been known that levels of plasma gelsolin can be depleted during acute pneumonia in humans, but no previous studies had directly shown evidence that it could enhance bacterial killing functions.  This interesting study demonstrated plasma gelsolin could increase the rate at which macrophages ingest bacteria as well as increase the efficiency of killing the bacteria once engulfed.  Importantly, these effects were via direct actions on the macrophages and not caused by simple opsonization of the bacteria.  In mechanistic studies, they demonstrated the ability of plasma gelsolin to upregulate NOS3, an enzyme necessary for synthesis of reactive nitrogen intermediates necessary for intracellular bacterial killing.  Using murine models, the investigators demonstrated that pre-treatment with plasma gelsolin could improve host defense and protect mice against lethal bacterial pneumonia.  Clearly more work needs to be done to determine whether plasma gelsolin can have beneficial effects if given after infection, but there is one clinical scenario where bacterial infection can be predicted, and that is in the case of pneumonia which often occurs about a week following influenza infection.  This study suggests that patients at high risk for bacterial complication of influenza infection could be treated prophylactically with plasma gelsolin to improve their chances of surviving post-viral secondary pneumonia.  Thus, this is a particularly encouraging study for a major clinical problem.

Bethany Moore

Associate Editor

AJP-Lung