PMID- 8156788
OWN - NLM
STAT- MEDLINE
DCOM- 19940519
LR  - 20190914
IS  - 0277-3740 (Print)
IS  - 0277-3740 (Linking)
VI  - 13
IP  - 2
DP  - 1994 Mar
TI  - Increased interleukin-1 activity in the injured vitamin A-deficient cornea.
PG  - 156-66
AB  - Injury to a vitamin A-deficient cornea leads to severe acute inflammation often 
      culminating in ulceration. We report on possible regulatory mechanisms involved 
      in the pathogenesis of corneal inflammation in vitamin A deficiency. Thymocyte 
      comitogenic assay and interleukin (IL)-6 induction in corneal fibroblasts have 
      shown that thermally injured and mechanically abraded vitamin A-deficient rat 
      corneas produce much higher levels of an IL-1-like factor as compared with 
      uninjured or injured, normal control corneas. This was confirmed by antibody 
      capture enzyme immunoassay, which detected high levels of IL-1 alpha and IL-1 
      beta in injured vitamin A-deficient corneas. To our knowledge this is the first 
      report describing the induction of IL-1 in the vitamin A-deficient cornea by 
      thermal and mechanical injuries. When mechanically injured corneas were screened 
      for chemotactic activity, they were found to contain significantly higher levels 
      of a chemoattractant as compared with similarly injured, normal control corneas. 
      Chemotactic activity [expressed as a percentage of a known chemotactic 
      tripeptide, formyl-methionyl-leucyl-phenylalanine (fMLP), found in medium 
      harvested from vitamin A-deficient corneas] averaged 58.8 +/- 8.9% (SEM) as 
      compared with 12.6 +/- 5.4% in medium conditioned by normal corneas. Checkerboard 
      analysis confirmed that the activity in vitamin A-deficient cornea conditioned 
      medium was chemotactic and not chemokinetic. These results demonstrate a 
      correlation between IL-1 levels and severity of inflammation in the injured 
      vitamin A-deficient rat cornea.
FAU - Shams, N B
AU  - Shams NB
AD  - Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical 
      School, Boston, Massachusetts 02114.
FAU - Reddy, C V
AU  - Reddy CV
FAU - Watanabe, K
AU  - Watanabe K
FAU - Elgebaly, S A
AU  - Elgebaly SA
FAU - Hanninen, L A
AU  - Hanninen LA
FAU - Kenyon, K R
AU  - Kenyon KR
LA  - eng
GR  - EY 05799/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  - United States
TA  - Cornea
JT  - Cornea
JID - 8216186
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-6)
SB  - IM
MH  - Animals
MH  - Chemotaxis, Leukocyte/*immunology
MH  - Cornea/*immunology/pathology
MH  - Corneal Ulcer/immunology/pathology
MH  - Fibroblasts/metabolism
MH  - Interleukin-1/*biosynthesis
MH  - Interleukin-6/biosynthesis
MH  - Male
MH  - Mice
MH  - Mice, Inbred C3H
MH  - Neutrophils/immunology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Vitamin A Deficiency/*immunology/pathology
EDAT- 1994/03/01 00:00
MHDA- 1994/03/01 00:01
CRDT- 1994/03/01 00:00
PHST- 1994/03/01 00:00 [pubmed]
PHST- 1994/03/01 00:01 [medline]
PHST- 1994/03/01 00:00 [entrez]
AID - 10.1097/00003226-199403000-00009 [doi]
PST - ppublish
SO  - Cornea. 1994 Mar;13(2):156-66. doi: 10.1097/00003226-199403000-00009.