PMID- 7781745
OWN - NLM
STAT- MEDLINE
DCOM- 19950714
LR  - 20190816
IS  - 0014-4835 (Print)
IS  - 0014-4835 (Linking)
VI  - 60
IP  - 2
DP  - 1995 Feb
TI  - Inflammation induced changes in adenosine 3',5'-cyclic monophosphate production 
      by ciliary epithelial cell bilayers.
PG  - 165-71
AB  - Despite extensive evidence implicating the cytokines interleukin-1 (IL-1) and 
      tumor necrosis factor-alpha (TNF alpha) in the intraocular inflammatory response, 
      little is known about their effects on signal transduction in anterior uveal 
      tissue. Since these cytokines have been shown to alter the adenylyl cyclase 
      system in nonocular tissues, we tested the hypothesis that IL-1 beta and TNF 
      alpha affect the anterior uvea by altering production of the intracellular second 
      messenger adenosine 3',5'-cyclic monophosphate (cAMP) in ciliary epithelial 
      bilayers. This was accomplished by measuring the levels of cAMP in bilayers ex 
      vivo, following intraocular inflammation induced by intravitreal injection of 
      IL-1 beta, TNF alpha or bacterial endotoxin, and in vitro, following exposure to 
      IL-1 beta, TNF alpha or bacterial endotoxin. Although cAMP production was 
      enhanced in bilayers from IL-1 beta-, TNF alpha- or endotoxin-inflamed eyes, ex 
      vivo, exposure of normal bilayers to IL-1 beta (15 U ml-1), TNF alpha (20 U 
      ml-1), or a low concentration of endotoxin (0.01 microgram ml-1) for 4 hr, in 
      vitro, had no effect on cAMP production. The inability of IL-1 beta, TNF alpha, 
      or the low concentration of endotoxin to increase cAMP production by bilayers, in 
      vitro, suggests that the enhanced cAMP production observed with inflamed 
      bilayers, ex vivo, was not due to a direct action of these inflammatory agonists 
      on the ciliary epithelial bilayer. Although direct exposure to cytokines or 
      endotoxin did not change cAMP production, treatment with IL-1 beta, TNF alpha, or 
      a higher concentration of endotoxin (1 microgram ml-1) did affect signal 
      transduction mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)
FAU - Fleisher, L N
AU  - Fleisher LN
AD  - North Carolina State University, College of Veterinary Medicine, Department of 
      Anatomy, Physiological Sciences and Radiology, Raleigh 27606, USA.
FAU - Ferrell, J B
AU  - Ferrell JB
FAU - McGahan, M C
AU  - McGahan MC
LA  - eng
GR  - EY08688/EY/NEI 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  - England
TA  - Exp Eye Res
JT  - Experimental eye research
JID - 0370707
RN  - 0 (Interleukin-1)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 1F7A44V6OU (Colforsin)
RN  - E0399OZS9N (Cyclic AMP)
RN  - L628TT009W (Isoproterenol)
SB  - IM
MH  - Animals
MH  - Ciliary Body/drug effects/*metabolism
MH  - Colforsin/pharmacology
MH  - Culture Techniques
MH  - Cyclic AMP/*biosynthesis
MH  - Epithelium/drug effects/metabolism
MH  - Interleukin-1/pharmacology
MH  - Isoproterenol/pharmacology
MH  - Lipopolysaccharides/pharmacology
MH  - Male
MH  - Rabbits
MH  - Recombinant Proteins/pharmacology
MH  - Tumor Necrosis Factor-alpha/pharmacology
MH  - Uveitis, Anterior/etiology/*metabolism
EDAT- 1995/02/01 00:00
MHDA- 1995/02/01 00:01
CRDT- 1995/02/01 00:00
PHST- 1995/02/01 00:00 [pubmed]
PHST- 1995/02/01 00:01 [medline]
PHST- 1995/02/01 00:00 [entrez]
AID - 10.1016/s0014-4835(95)80007-7 [doi]
PST - ppublish
SO  - Exp Eye Res. 1995 Feb;60(2):165-71. doi: 10.1016/s0014-4835(95)80007-7.