In response to infectious and, in some instances, noninfectious insults, the 
affected tissues/cells of the host undergo inflammation. However, uncontrolled 
inflammation could be detrimental to the host, resulting in inflammatory 
disease, such as inflammatory lung disease. Although the etiology of the disease 
is well defined, the underling pathogenesis is still incompletely understood. 
The renin-angiotensin system (RAS), one of the primary cardiovascular regulatory 
systems, has been proposed to be involved in the pathogenesis of inflammatory 
lung disease. In particular, the RAS has been implicated as advances in the 
understanding of the multifunctionality of individual components of the system 
have been made, and by the fact that the RAS acts not only systemically, but 
also locally in a variety of tissues, including the lung. Angiotensin-converting 
enzyme 2 (ACE2), a relatively new member of the RAS, has drawn extensive 
attention since 2003, because of the findings that ACE2 is the receptor for SARS 
Corona virus and that maintenance of normal ACE2 levels in the lung is 
beneficial for the host to combat inflammatory lung disease. Nevertheless, the 
mechanism through which ACE2 plays a role in inflammatory lung disease has not 
been clearly identified. In an attempt to summarize current literature findings 
and progress made in uncovering the role of ACE2 in inflammatory lung disease, 
this review will focus on recent studies examining pulmonary ACE2 biology, its 
roles in inflammatory lung disease pathogenesis and possible underlying 
mechanisms. Finally, we will discuss pulmonary ACE2 as a potential therapeutic 
target for inflammatory lung disease.