|
Respir Med. 2005 Sep;99(9):1145-51.
Epub 2005 Mar 25. |
Comparison
of BALF concentrations of ENA-78 and IP10 in patients with idiopathic pulmonary
fibrosis and nonspecific interstitial pneumonia.
Nakayama S, Mukae
H, Ishii H, Kakugawa
T, Sugiyama K, Sakamoto N, Fujii
T, Kadota
J, Kohno S.
Second Department of Internal Medicine,
BACKGROUND: Epithelial neutrophil-activating peptide
78 (ENA-78) and interferon gamma-inducible protein 10 (IP10) belong to the CXC chemokine family and are considered to be important factors
in idiopathic pulmonary fibrosis (IPF). Idiopathic nonspecific interstitial
pneumonia (NSIP) and IPF are the two largest subsets of idiopathic interstitial
pneumonias (IIP). In patients with NSIP, the prognosis is generally good
compared with IPF. Therefore, the pathogenesis of NSIP seems to be different
from that of IPF, but this remains unclear. The aim of the present study was to
evaluate the contribution of ENA-78 and IP10 in the two diseases. METHODS: We
measured the levels of ENA-78 and IP10 in serum and bronchoalveolar
lavage fluid (BALF) of patients with IPF (n=17),
idiopathic NSIP (n=10) and healthy subjects (n=12) by enzyme-linked immunosorbent assays. RESULTS: The level of ENA-78 in BALF
was significantly higher in IPF patients than in NSIP patients and controls.
Serum levels of ENA-78 and BALF levels of IP10 in NSIP patients were
significantly higher than in patients with IPF and controls. In BALF of
patients with NSIP, IP10 level significantly correlated with the absolute
number of lymphocytes. In IPF patients, BALF IP10 levels also correlated with
the proportion of lymphocytes in BALF. CONCLUSION: Our results show distinct
profiles of CXC chemokines in IPF and NSIP, and
suggest that these chemokines play an important role
in inflammatory cell recruitment into the lung in patients with IIP.
|
Immunology.
2006 Jan;117(1):11-21. |
Toll-like receptor 3
agonist poly(I:C)-induced antiviral response in human
corneal epithelial cells.
Kumar
A, Zhang J, Yu FS.
Kresge Eye Institute/Department of Ophthalmology,
Wayne State University School of Medicine, Detroit, MI 48201, USA.
The objective of this study was to examine the expression of Toll-like receptor
3 (TLR3) by human corneal epithelial cells (HCECs)
and to determine whether exposure to the TLR3 agonist polyinosinic-polycytidylic
acid [poly(I:C)] induces an antiviral response in
these cells. Fluorescence-activated cell sorter (FACS) analysis revealed TLR3
to be constitutively expressed and distributed intracellularly
in HCECs. Stimulation of HCECs
with the TLR3 agonist poly(I:C) induced the activation
of nuclear factor (NF)-kappaB and production of the proinflammatory cytokine interleukin (IL)-6 and the chemokine IL-8. Upon exposure to poly(I:C),
HCECs initiated a potent antiviral response resulting
in an increase of interferon (IFN)-beta mRNA expression (7-fold). Poly(I:C) stimulation also up-regulated mRNA expression of
the antiviral chemokine IFN-gamma inducible protein
10 (IP10), myxovirus resistance gene A and
2',5'-oligoadenylate synthetase (5-, 10- and 9-fold,
respectively), and secretion of IP10. These responses were also induced by
exogenously added type 1 IFNs, but could not be
blocked by pretreatment of the cells with anti-TLR3 monoclonal antibody,
suggesting that the receptor was not expressed on the cell surface.
Furthermore, incubation of HCECs with an endosomal acidification inhibitor, chloroquine,
markedly inhibited poly(I:C)-mediated IFN-beta
expression in HCECs. These results suggest that
corneal epithelial cells are important sentinels of the corneal innate immune
system against viral infection, and that stimulation of TLR3 can induce the
expression of key proinflammatory cytokines and chemokines and antiviral genes that help in the defence of the cornea against viral infection.
PMID: 16423036 [PubMed - indexed for MEDLINE]