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Distribution of intercellular adhesion molecule-1 on leukocytes and corneal endothelium after endotoxin stimulation
K Yamaguchi1, Y Takahashi, S Takahashi
1Department of Ophthalmology, Yamagata University School of Medicine, Japan.
Insights
Salmonella endotoxin increases intercellular adhesion molecule-1 (ICAM-1) on rat corneal endothelium and leukocytes. This heightened ICAM-1 may promote leukocyte adhesion to the cornea.
Area of Science:
- Ophthalmology
- Immunology
- Cell Biology
Background:
- Intercellular adhesion molecule-1 (ICAM-1) plays a role in immune cell interactions.
- Understanding ICAM-1 expression in ocular tissues is crucial for inflammatory eye conditions.
Purpose of the Study:
- To investigate the effect of Salmonella typhimurium endotoxin on ICAM-1 expression in rat corneal endothelium and leukocytes.
- To elucidate the topographical distribution of ICAM-1 on these cells post-endotoxin stimulation.
Main Methods:
- Lewis rats were injected with Salmonella typhimurium endotoxin.
- Corneal tissues were collected at 0 and 16 hours post-injection.
- Immunoscanning electron microscopy was employed to visualize ICAM-1 distribution.
Main Results:
- ICAM-1 was detected on cytoplasmic processes of corneal endothelial cells, particularly along microfolds.
- In leukocytes, ICAM-1 was predominantly found on non-specialized cell body surfaces.
- Endotoxin stimulation led to increased ICAM-1 expression in both corneal endothelium and leukocytes.
Conclusions:
- Salmonella endotoxin significantly upregulates ICAM-1 expression in the cornea.
- Elevated ICAM-1 levels likely contribute to leukocyte clustering and adhesion to the corneal endothelium.
- This finding provides insights into the inflammatory mechanisms in endotoxin-induced ocular responses.
Abstract:
After stimulation with Salmonella typhimurium endotoxin, the intercellular adhesion molecule-1 (ICAM-1) was studied on the corneal endothelium and associated leukocytes in rats using immunoscanning electron microscopy. Two hundred micrograms of the endotoxin was injected in Lewis rats. The corneae were excised at 0-h and 16-h-postinjection time (n = 5, respectively). The corneae were prepared in hypothermic University of Wisconsin (UW) solution for immunoscanning electron microscopy. Histotopographical examination visualized ICAM-1 antigen on cytoplasmic processes of the corneal endothelium, arranged along microfolds, especially at the peaks. In the leukocytes, ICAM-1 was located primarily in morphologically non-specialized domains of the cell body surface, and only rarely scattered on the surface of microvillar projections. We concluded that the endotoxin stimulation can increase ICAM-1 in both corneal endothelium and associated leukocytes. Increased ICAM-1 may be an important factor for the leukocytes to form clustering and adhering to the corneal endothelium.