How to Nominate a Candidate for the AJP-Lung Young Investigator Award: Infographic

The deadline has been extended to April 1 2014.  The award is posted on the APS website here.  Send us a nomination! 

Quantum dot technology reveals involvement of endothelial NOX2 in VCAM expression

Please see the fascinating article by Dr. Orndorff et al. published in AJP-Lung and selected for inclusion in APS Select.  Dr. Orndorff and her collaborators attached antibodies against VCAM and PECAM to fluorescent quantum dots to pinpoint the sequence of events leading to the sticking and activated neutrophils on endothelial cells.  Their data show for the first time that in LPS induced injury reactive species generated by endothelial NOX2  (in addition to neutrophil NOX2) upregulate VCAM  causing neutrophil to stick to endothelial cells and produce reactive intermediates which damage endothelial cells.  Please see the highly informative (and colorful) figures in this article here.  The authors should be congratulated for their highly innovative study.

It is fair to say that there is still some controversy as to the extent to which neutrophils contribute to the pathogenesis of ARDS-type injury in both humans and animals.  Of note, Dr. Gessner et al. showed that exposure of mice to oxidant gases damaged neutrophils decreasing their ability to generate reactive intermediates in their June 2013 article. Please also see the review by Drs. William and Chambers on “The mercurial nature of neutrophils: still an enigma in ARDS?” recently published in AJP-Lung.

James Noah on Camels and MERS

Dr. James Noah, an infectious disease specialist at the Southern Research Institute, posted the following response to this recent New York Times article on Middle Eastern Respiratory Syndrome (MERS) on our Facebook page:

Zoonesis occurs any time that a disease transmits naturally from a vertebrate animal to a human.  This process happens every day with bacteria, parasites, fungi, and viruses.  In the viral world, a sustained and re-occurring zoonesis is seen with influenza viruses, where humans and animals trade different strains frequently.  An example of a terminal zoonesis would be rabies, which is tolerated in animals but is close to 100% fatal in humans.  New examples of zooneses are increasingly observed (likely due to our increasingly advanced surveillance programs), and when they do, there is a quiet but determined search for the animal reservoir of the emerging pathogen.  In 2012, Middle East Respiratory Syndrome (MERS) emerged with a high human mortality, and last month a putative reservoir for the virus was identified in camels.  Camels are used for transportation, entertainment, and food in the affected regions of the Middle East. They also have a high infection rate for MERS and may be responsible for the unexplained spread of the respiratory virus. However, they appear to be asymptomatic when infected, and this may pose a problem for disease containment and control.  I agree with Dr. Lipkin's assessment; how do you identify respiratory virus symptoms in a slobbering, spitting camel?

Adapting global influenza management strategies to address emerging viruses is a related AJP-Lung article from July 2013 by Dr. Noah and his wife, Diana L. Noah.

The Possible Role of Statins in a Flu Pandemic

The good news: this winter’s wave of flu cases has finally started to decline. The bad news: high-mortality, novel strains of influenza continue to arise (e.g. H7N9), raising the specter of a major pandemic if they acquire greater transmissibility from person-to-person.

A recent online article here discusses the possible use of statins to reduce mortality in a pandemic scenario, and includes comments by one of our AJP-Lung Associate editors, Dr.Lester Kobzik. 

  

AJP-Lung has been contributing to the scientific progress on this topic, with a review and several relevant articles in 2013 alone: 

Autophagy mediates avian influenza H5N1 pseudotyped particle-induced lung inflammation through NF-κB andp38 MAPK signaling pathways.

                             

Neonatal hyperoxia alters the host response to influenza A virus infection in adult mice through multiplepathways.

                                               

Adapting global influenza management strategies to address emerging viruses.

               

FABP5 deficiency enhances susceptibility to H1N1 influenza A virus-induced lung inflammation.

                               

Compromised respiratory function in lethal influenza infection is characterized by the depletion oftype I alveolar epithelial cells beyond threshold levels.

               

Influenza matrix protein 2 alters CFTR expression and function through its ion channel activity.

                

What do you think about this?  Care to tell us in the comments?