title: Modulatory effect of sera from patients with various types of pulmonary fibrosis on mononuclear cell induced angiogenesis in relation to pulmonary function.
abstract: Angiogenesis plays an important role in the pathogenesis of idiopathic pulmonary fibrosis. Pulmonary fibrosis occurs also in many diseases, such as other types of interstitial pneumonias or drug-induced pulmonary fibrosis. The aim of the study was to examine the effect of sera from patients with various types of pulmonary fibrosis on angiogenesis induced by human mononuclear cells (MNC) in relation to lung functions. The study population consisted of 32 patients with idiopathic pulmonary fibrosis (IPF), 11 patients with drug-induced pulmonary fibrosis (DIPF), 6 with cryptogenic organizing pneumonia (COP), and 20 healthy volunteers. An animal model of leukocyte-induced angiogenesis assay was used as an angiogenic test. Spirometry, whole-body plethysmography, static lung compliance (Cst), and diffusing capacity of the lung for CO (DL(CO)) were performed in all patients. Sera from IPF and COP patients significantly stimulated angiogenic activity of MNC, compared with sera from healthy donors and from DIPF patients (P<0.001). However, sera from healthy donors and DIPF significantly stimulated angiogenic activity of MNC compared with the control group with PBS (P<0.001). In all groups, a decrease in the mean value of Cst and DL(CO) was observed, but no significant correlation between VC, FEV(1), DL(CO), Cst, and angiogenic activity of sera from examined patients was found. Sera obtained from patients with pulmonary fibrosis constitute a source of mediators modulating angiogenesis, but the pattern of reaction is different in various diseases. The strongest reaction is observed in IPF and the weakest one in DIPF. The angiogenic activity of sera did not correlate with the pulmonary function of patients with pulmonary fibrosis.
authors.affiliation: Department of Family Medicine, Warsaw Medical University, Warsaw, Poland. tmzielonka@wp.pl
authors.forename: T M
authors.initials: TM
authors.lastname: Zielonka
authors.forename: U
authors.initials: U
authors.lastname: Demkow
authors.forename: M
authors.initials: M
authors.lastname: Filewska
authors.forename: B
authors.initials: B
authors.lastname: Bialas-Chromiec
authors.forename: K
authors.initials: K
authors.lastname: Zycinska
authors.forename: J
authors.initials: J
authors.lastname: Szopinski
authors.forename: P
authors.initials: P
authors.lastname: Remiszewski
authors.forename: E
authors.initials: E
authors.lastname: Rowinska-Zakrzewska
authors.forename: K A
authors.initials: KA
authors.lastname: Wardyn
authors.forename: E
authors.initials: E
authors.lastname: Skopinska-Rozewska
mesh_terms: D000328:Adult; D000368:Aged; D000818:Animals; D005260:Female; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000502:physiology*; D008168:Lung / Q000503:physiopathology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008875:Middle Aged; D009389:Neovascularization, Pathologic / Q000473:pathology*; D011658:Pulmonary Fibrosis / Q000097:blood* / Q000139:chemically induced / Q000503:physiopathology*; D012129:Respiratory Function Tests