PMID- 9927365
OWN - NLM
STAT- MEDLINE
DCOM- 19990305
LR  - 20151119
IS  - 1073-449X (Print)
IS  - 1073-449X (Linking)
VI  - 159
IP  - 2
DP  - 1999 Feb
TI  - Pentoxifylline inhibits TNF-alpha production from human alveolar macrophages.
PG  - 508-11
AB  - Tumor necrosis factor-alpha (TNF-alpha) is an important proinflammatory cytokine. 
      Recently, pentoxifylline (POF) has been shown to suppress the synthesis of 
      TNF-alpha from lipopolysaccharide (LPS)-stimulated human monocytes in cell 
      cultures and in vivo. The aim of this study was to investigate whether 
      POF-induced suppression of TNF-alpha secretion affects peripheral blood monocytes 
      (PBM) and alveolar macrophages (AM) equally, and whether POF is able to suppress 
      the spontaneous TNF-alpha production from AM in pulmonary sarcoidosis in vitro. 
      In seven patients without interstitial lung disease we studied the effect of POF 
      on LPS-stimulated PBM and AM cultured for 24 h. In six patients with sarcoidosis 
      we investigated the effect of POF on the enhanced spontaneous TNF-alpha 
      production by AM in vitro. POF induced a dose-dependent suppression of the 
      LPS-stimulated TNF-alpha production which was not different for PBM and AM, 
      respectively. In sarcoidosis, POF inhibited the spontaneous TNF-alpha production 
      of AM at 0.1 mM by 91% and at 1 mM by 98%. In conclusion, POF inhibits 
      LPS-induced TNF-alpha production from PBM and AM to a similar extent and can also 
      inhibit the exaggerated spontaneous TNF-alpha production from AM in sarcoidosis 
      in vitro. This may be the basis for further clinical trials to evaluate POF as an 
      immunotherapeutic agent in sarcoidosis.
FAU - Marques, L J
AU  - Marques LJ
AD  - Department of Pneumology and Allergy, Ruhrlandklinik, Medical Faculty, University 
      of Essen, Germany.
FAU - Zheng, L
AU  - Zheng L
FAU - Poulakis, N
AU  - Poulakis N
FAU - Guzman, J
AU  - Guzman J
FAU - Costabel, U
AU  - Costabel U
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Am J Respir Crit Care Med
JT  - American journal of respiratory and critical care medicine
JID - 9421642
RN  - 0 (Biomarkers)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Phosphodiesterase Inhibitors)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - SD6QCT3TSU (Pentoxifylline)
SB  - IM
MH  - Adult
MH  - Biomarkers
MH  - Cells, Cultured
MH  - Dose-Response Relationship, Drug
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Humans
MH  - Lipopolysaccharides/pharmacology
MH  - Macrophages, Alveolar/drug effects/*metabolism/pathology
MH  - Male
MH  - Middle Aged
MH  - Pentoxifylline/*pharmacology
MH  - Phosphodiesterase Inhibitors/*pharmacology
MH  - Sarcoidosis, Pulmonary/drug therapy/metabolism/pathology
MH  - Tumor Necrosis Factor-alpha/*antagonists & inhibitors/biosynthesis
EDAT- 1999/02/02 00:00
MHDA- 1999/02/02 00:01
CRDT- 1999/02/02 00:00
PHST- 1999/02/02 00:00 [pubmed]
PHST- 1999/02/02 00:01 [medline]
PHST- 1999/02/02 00:00 [entrez]
AID - 10.1164/ajrccm.159.2.9804085 [doi]
PST - ppublish
SO  - Am J Respir Crit Care Med. 1999 Feb;159(2):508-11. doi: 
      10.1164/ajrccm.159.2.9804085.