Different angiogenic activity in pulmonary sarcoidosis and idiopathic pulmonary fibrosis.
BACKGROUND
Recent evidence has shown that several chemokines--including those involved in angiogenesis--have been implicated in the pathogenesis of idiopathic pulmonary fibrosis (IPF) and sarcoidosis. We speculated that these differences could be attributed to distinct angiogenic and angiostatic profiles. This hypothesis was investigated by estimating the levels of three angiogenic chemokines (growth-related gene [GRO]-alpha, epithelial neutrophil-activating protein [ENA]-78, and interleukin [IL]-8), and three angiostatic chemokines (monokine induced by interferon (IFN)-gamma [MIG], IFN-gamma-inducible protein [IP]-10, and IFN-gamma-inducible T-cell alpha chemoattractant) in serum and BAL fluid (BALF).


METHODS
We studied prospectively 20 patients with sarcoidosis (median age, 46 years; range, 25 to 65 years), 20 patients with IPF (median age, 68 years; range, 40 to 75 years), and 10 normal subjects (median age, 39 years; range, 26 to 60 years).


RESULTS
The GRO-a serum and BALF levels of IPF patients were found significantly increased in comparison with healthy subjects (799 pg/mL vs 294 pg/mL [p = 0.022] and 1,827 pg/mL vs 94 pg/mL [p < 0.001], respectively) and sarcoidosis patients (799 pg/mL vs 44 pg/mL [p < 0.001] and 1,827 pg/mL vs 214 pg/mL [p < 0.001], respectively). Moreover, ENA-78 and IL-8 BALF levels in IPF patients were significantly higher compared with sarcoidosis patients (191 pg/mL vs 30 pg/mL [p < 0.001] and 640 pg/mL vs 94 pg/mL [p = 0.03], respectively). MIG serum levels in IPF patients were found significantly upregulated in comparison with sarcoidosis patients and healthy control subjects. However, MIG and IP-10 BALF levels (1,136 pg/mL vs 66 pg/mL [p < 0.001] and 112 pg/mL vs 56 pg/mL [p = 0.037], respectively) were significantly higher in sarcoidosis patients compared with IPF patients.


CONCLUSIONS
Our data suggest distinct angiogenic profiles between IPF and sarcoidosis, indicating a potential different role of CXC chemokines in the local immunologic response in IPF and pulmonary sarcoidosis.
Antoniou
Katerina M
KM
Department of Thoracic Medicine, University Hospital, Medical School, University of Crete, Heraklion 71110 Crete, Greece.
Tzouvelekis
Argyris
A
Alexandrakis
Michael G
MG
Sfiridaki
Katerina
K
Tsiligianni
Ioanna
I
Rachiotis
George
G
Tzanakis
Nikolaos
N
Bouros
Demosthenes
D
Milic-Emili
Joseph
J
Siafakas
Nikolaos M
NM
D000328:Adult; D000368:Aged; D043165:Angiostatic Proteins / Q000032:analysis; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D054360:Chemokine CXCL1; D054357:Chemokine CXCL10; D054365:Chemokine CXCL5; D054370:Chemokine CXCL9; D018925:Chemokines / Q000032:analysis*; D019743:Chemokines, CXC / Q000032:analysis*; D005260:Female; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins / Q000032:analysis*; D016209:Interleukin-8 / Q000032:analysis*; D008168:Lung / Q000276:immunology / Q000473:pathology; D008297:Male; D008875:Middle Aged; D011658:Pulmonary Fibrosis / Q000276:immunology / Q000473:pathology*; D012016:Reference Values; D017565:Sarcoidosis, Pulmonary / Q000276:immunology / Q000473:pathology*
D043165:Angiostatic Proteins; C475829:CXCL1 protein, human; C114753:CXCL10 protein, human; C486263:CXCL5 protein, human; C080810:CXCL9 protein, human; D054360:Chemokine CXCL1; D054357:Chemokine CXCL10; D054365:Chemokine CXCL5; D054370:Chemokine CXCL9; D018925:Chemokines; D019743:Chemokines, CXC; D036341:Intercellular Signaling Peptides and Proteins; D016209:Interleukin-8