Sc. Bellum et al., EXPERIMENTAL REOVIRUS SEROTYPE-1 STRAIN LANG INFECTION OF THE LUNG - A MODEL FOR THE STUDY OF THE LUNG IN THE CONTEXT OF MUCOSAL IMMUNITY, Laboratory investigation, 74(1), 1996, pp. 221-231
A number of studies have examined the nature of the respiratory immune
response to particular pathogens. Although many pathogens stimulate s
pecific immunity in the lung, they frequently are not effective immuno
gens at other mucosal sites. Because the gastrointestinal tract is a m
ajor inductive site for mucosal immunity, a pathogen that is an effect
ive respiratory and gut immunogen would allow studies of the interacti
on of the lung with gut mucosal immune system. Reovirus, a respiratory
isolate that previously has been shown to be an effective gut mucosal
immunogen, provides a potential model of the relationship of the lung
to the gut mucosal immune system. In this report, we demonstrate that
intranasal application of reovirus serotype 1/strain Lang (1/L) to CD
-1 mice elicits an acute lymphocytic inflammatory infiltration of the
lung and hyperplasia of the lung-associated lymph nodes. The initial i
nflammatory response occurs in the airspaces and interstitium of the l
ung. As the infection progresses, the initially diffuse cellular infil
trate becomes more focused around small bronchioles. Viral replication
occurs predominantly during the first week of the infection, and infe
ctious virions are eliminated during the second week. After the elimin
ation of infectious virions, a secondary response consisting of the ap
pearance of plasma cells adjacent to pulmonary arteries develops as th
e primary infiltrate organizes into peribronchiolar follicles, resembl
ing the human inflammatory lung condition termed follicular bronchioli
tis. These two infiltration patterns were also observed by immunohisto
chemical analysis of the the infected lung. Whereas CD4+ and CD8+ lymp
hocytes and Mac-1+ cells were found to be more closely associated with
the primary infiltration process, B220+ lymphocytes were observed adj
acent to pulmonary arteries. These results establish respiratory reovi
rus 1/L infection as a viable model for future investigations of the m
ucosal immune response in the lung and its relationship to the common
mucosal immune system.