PMID- 14507654
OWN - NLM
STAT- MEDLINE
DCOM- 20031029
LR  - 20181113
IS  - 0002-9440 (Print)
IS  - 1525-2191 (Electronic)
IS  - 0002-9440 (Linking)
VI  - 163
IP  - 4
DP  - 2003 Oct
TI  - Respiratory reovirus 1/L induction of intraluminal fibrosis, a model of 
      bronchiolitis obliterans organizing pneumonia, is dependent on T lymphocytes.
PG  - 1467-79
AB  - Bronchiolitis obliterans organizing pneumonia (BOOP) is a clinical syndrome 
      characterized by perivascular/peribronchiolar leukocyte infiltration leading to 
      the development of intraalveolar fibrosis. We have developed an animal model of 
      BOOP where CBA/J mice infected with 1 x 10(6) plaque-forming units (PFU) reovirus 
      1/L develop follicular bronchiolitis and intraalveolar fibrosis similar to human 
      BOOP. In this report, we demonstrate a role for T cells in the development of 
      intraluminal fibrosis associated with BOOP. Corticosteroid treatment of reovirus 
      1/L-infected mice both inhibited the development of fibrotic lesions when 
      administered early in the time-course and promoted the resolution of fibrotic 
      lesions when corticosteroid administration was delayed. Further, the depletion of 
      either CD4(+) or CD8(+) T cells before reovirus 1/L infection also inhibited 
      fibrotic lesion development. Both corticosteroid treatment and depletion of 
      CD4(+) or CD8(+) T cells also resulted in decreased expression of the 
      proinflammatory and profibrotic cytokines, interferon (IFN)-gamma and monocyte 
      chemoattractant protein-1 (MCP-1). Further, treatment of mice with a neutralizing 
      monoclonal antibody to IFN-gamma also significantly inhibited the development of 
      fibrosis. Taken together, these results suggest a significant role for T cells in 
      the development of reovirus 1/L-induced BOOP fibrotic lesions in CBA/J mice and 
      suggests that T(H)1-derived cytokines, especially IFN-gamma, may play a key role 
      in fibrotic lesion development.
FAU - Majeski, Elizabeth I
AU  - Majeski EI
AD  - Department of Microbiology and Immunology, Medical University of South Carolina, 
      Charleston, South Carolina 29425, USA.
FAU - Paintlia, Manjeet K
AU  - Paintlia MK
FAU - Lopez, Andrea D
AU  - Lopez AD
FAU - Harley, Russell A
AU  - Harley RA
FAU - London, Steven D
AU  - London SD
FAU - London, Lucille
AU  - London L
LA  - eng
GR  - AI R01 40175/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Pathol
JT  - The American journal of pathology
JID - 0370502
RN  - 0 (Chemokines)
RN  - 0 (Cytokines)
RN  - 0 (Glucocorticoids)
RN  - X4W7ZR7023 (Methylprednisolone)
SB  - IM
MH  - Animals
MH  - Bronchoalveolar Lavage Fluid/cytology
MH  - CD4-Positive T-Lymphocytes/pathology
MH  - CD8-Positive T-Lymphocytes/pathology
MH  - Chemokines/metabolism
MH  - Cryptogenic Organizing Pneumonia/pathology/*physiopathology
MH  - Cytokines/metabolism
MH  - Disease Models, Animal
MH  - Female
MH  - Fibrosis
MH  - Glucocorticoids/pharmacology
MH  - Humans
MH  - Inflammation/pathology
MH  - Leukapheresis
MH  - Lung/drug effects/metabolism/pathology
MH  - Methylprednisolone/pharmacology
MH  - Mice
MH  - Mice, Inbred CBA
MH  - Nasal Cavity/virology
MH  - *Orthoreovirus, Mammalian
MH  - Pulmonary Fibrosis/pathology/*physiopathology/*virology
MH  - Reoviridae Infections/*complications
MH  - *T-Lymphocytes
PMC - PMC1868312
EDAT- 2003/09/26 05:00
MHDA- 2003/10/30 05:00
PMCR- 2004/04/01
CRDT- 2003/09/26 05:00
PHST- 2003/09/26 05:00 [pubmed]
PHST- 2003/10/30 05:00 [medline]
PHST- 2003/09/26 05:00 [entrez]
PHST- 2004/04/01 00:00 [pmc-release]
AID - S0002-9440(10)63504-3 [pii]
AID - 3829 [pii]
AID - 10.1016/S0002-9440(10)63504-3 [doi]
PST - ppublish
SO  - Am J Pathol. 2003 Oct;163(4):1467-79. doi: 10.1016/S0002-9440(10)63504-3.