| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Division of Pulmonary, Critical Care, and Occupational Medicine, University of Iowa College of Medicine and Veterans Administrations Medical Center, Iowa City, IA 52242
Hypersensitivity pneumonitis (HP) is a granulomatous, inflammatory
lung disease caused by inhalation of organic Ags, most commonly
thermophilic actinomycetes that cause farmer’s lung disease. The early
response to Ag is an increase in neutrophils in the lung, whereas the
late response is a typical Th1-type granulomatous disease. Many
patients who develop disease report a recent viral respiratory
infection. These studies were undertaken to determine whether viruses
can augment the inflammatory responses in HP. C57BL/6 mice were exposed
to the thermophilic bacteria Saccharopolyspora
rectivirgula (SR) for 3 consecutive days per wk for 3 wk. Some
mice were exposed to SR at 2 wk after infection with respiratory
syncytial virus (RSV), whereas others were exposed to SR after exposure
to saline alone or to heat-inactivated RSV. SR-treated mice developed a
typical, early neutrophil response and a late granulomatous
inflammatory response. Up-regulation of IFN-
and IL-2 gene
expression was also found during the late response. These responses
were augmented by recent RSV infection but not by heat-inactivated RSV.
Mice with a previous RSV infection also had a greater early neutrophil
response to SR, with increased macrophage inflammatory protein-2
(MIP-2, murine equivalent of IL-8) release in bronchoalveolar lavage
fluid. These studies suggest that viral infection can augment both the
early and late inflammatory responses in HP.
This article has been cited by other articles:
|
|
 |
|
  M. Girard, E. Israel-Assayag, and Y. Cormier Mature CD11c+ cells are enhanced in hypersensitivity pneumonitis Eur. Respir. J., September 1, 2009; 34(3): 749 - 756. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. L. Bustos, S. Frias, S. Ramos, A. Estrada, J. L. Arreola, F. Mendoza, M. Gaxiola, M. Salcedo, A. Pardo, and M. Selman Local and Circulating Microchimerism Is Associated with Hypersensitivity Pneumonitis Am. J. Respir. Crit. Care Med., July 1, 2007; 176(1): 90 - 95. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. J. Hwang, S. Kim, W. S. Park, and D. H. Chung IL-4-Secreting NKT Cells Prevent Hypersensitivity Pneumonitis by Suppressing IFN-{gamma}-Producing Neutrophils J. Immunol., October 15, 2006; 177(8): 5258 - 5268. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Selman, A. Pardo, L. Barrera, A. Estrada, S. R. Watson, K. Wilson, N. Aziz, N. Kaminski, and A. Zlotnik Gene Expression Profiles Distinguish Idiopathic Pulmonary Fibrosis from Hypersensitivity Pneumonitis Am. J. Respir. Crit. Care Med., January 15, 2006; 173(2): 188 - 198. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. N. Fink, H. G. Ortega, H. Y. Reynolds, Y. F. Cormier, L. L. Fan, T. J. Franks, K. Kreiss, S. Kunkel, D. Lynch, S. Quirce, et al. Needs and Opportunities for Research in Hypersensitivity Pneumonitis Am. J. Respir. Crit. Care Med., April 1, 2005; 171(7): 792 - 798. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M R Hill, L Briggs, M M Montano, A Estrada, G J Laurent, M Selman, and A Pardo Promoter variants in tissue inhibitor of metalloproteinase-3 (TIMP-3) protect against susceptibility in pigeon breeders' disease Thorax, July 1, 2004; 59(7): 586 - 590. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. S. Butler, M. M. Monick, T. O. Yarovinsky, L. S. Powers, and G. W. Hunninghake Altered IL-4 mRNA Stability Correlates with Th1 and Th2 Bias and Susceptibility to Hypersensitivity Pneumonitis in Two Inbred Strains of Mice J. Immunol., October 1, 2002; 169(7): 3700 - 3709. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
