Injection of chemoattractants into normal cornea: a model of inflammation after alkali injury.
OBJECTIVE
The objective of this study was to establish and characterize the invasion of polymorphonuclear leukocytes (PMNs) into a normal cornea after intrastromal injection of the tripeptide chemoattractants generated from alkali-degraded corneas.


METHODS
The following samples were injected into the midstroma of normal rabbit corneas: ultrafiltered tripeptide chemoattractants (N-acetyl-proline-glycine-proline and N-methyl-proline-glycine-proline) generated from alkali-degraded corneas, synthetic N-acetyl-PGP, positive control (leukotriene B4 [LTB4]), or negative control (Hanks' balanced salt solution [HBSS]). Timed responses of PMN infiltration were established for effective concentrations of LTB4 or the ultrafiltered chemoattractants.


RESULTS
All intrastromal injections resulted in the immediate development of an edematous disc that was 10 mm in diameter. The lesion essentially had cleared in the HBSS-injected eyes by 8 hours, and histologic sections revealed minimal numbers of PMNs in the cornea or limbal tissue. The injection of LTB4 or the ultrafiltered tripeptide chemoattractants induced peak numbers of PMNs within the stroma at 8 hours, subsiding by 16 hours. Seventy units of ultrafiltered chemoattractants yielded a strong PMN response, similar to 1 X 10(-5) M LTB4. The highest concentration of ultrafiltered chemoattractants (350 U) produced a severe PMN response that was characterized by a solid sheet of neutrophils surrounding the injection site. The injection of synthetic N-acetyl-PGP (2 X 10(-4) M) produced a marked PMN response.


CONCLUSIONS
PMN invasion of the normal cornea after the injection of the ultrafiltered tripeptide chemoattractants or the synthetic N-acetyl-PGP mimicked early PMN infiltration in the alkali-injured eye, confirming the importance of this chemoattractant as an inflammatory mediator.
Pfister
R R
RR
The Eye Research Laboratories, Brookwood Medical Center, Birmingham, Alabama, USA.
Haddox
J L
JL
Sommers
C I
CI
D000818:Animals; D002057:Burns, Chemical / Q000276:immunology / Q000473:pathology; D002630:Chemotactic Factors / Q000494:pharmacology*; D002634:Chemotaxis, Leukocyte; D003319:Corneal Stroma / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D004195:Disease Models, Animal; D005126:Eye Burns / Q000139:chemically induced / Q000473:pathology; D006801:Humans; D007267:Injections; D007634:Keratitis / Q000276:immunology* / Q000473:pathology; D007958:Leukocyte Count; D007975:Leukotriene B4 / Q000494:pharmacology; D009504:Neutrophils / Q000276:immunology* / Q000473:pathology; D009842:Oligopeptides / Q000494:pharmacology; D011817:Rabbits; D012972:Sodium Hydroxide / Q000009:adverse effects
D002630:Chemotactic Factors; D009842:Oligopeptides; D007975:Leukotriene B4; D012972:Sodium Hydroxide