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D. Zoukhri, E. Macari, C.L. Kublin; A Single Injection of Interleukin–1 Induces Reversible Lacrimal Gland Inflammation, Aqueous–Tear Deficiency, and Stimulates Acinar Cell Proliferation . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1938.
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© ARVO (1962-2015); The Authors (2016-present)
We have previously reported that a single injection of interleukin–1α (IL–1α) into the lacrimal gland inhibited both neurally– as well as agonist–induced protein secretions. The purpose of the present studies was to determine the effect of IL–1α on tear production and to determine if the inhibitory effect of IL–1α on lacrimal gland secretion is reversible.
IL–1α (1 µg) or saline (vehicle) was injected (2 µl) into the exorbital lacrimal glands of anesthetized female Balb/c or C57BL/6 mice. Animals were sacrificed 1–, 2–, 3–, or 7–days following the injection. The amount of tears in both eyes was measured using phenol red–impregnated cotton threads. The lacrimal glands were then removed and processed for histology, immunohistochemistry and measurement of protein secretion. Lacrimal gland sections were stained with hematoxylin–eosin or giemsa to determine the degree of inflammation. Cell proliferation was determined using an antibody against the nuclear antigen Ki67. To measure protein secretion, lacrimal gland lobules were stimulated for 20 min with high KCl buffer (to activate lacrimal gland nerve endings) followed by incubation for 20 min in the presence of phenylephrine (an adrenergic agonist) or carbachol (a cholinergic agonist).
Compared to saline injected Balb/c mice (4.3 ± 0.9 mm/10s), the amount of tears was significantly reduced following IL–1α injection at 1– (1.8 ± 0.3), 2– (2.5 ± 0.2), and 3–day (3.8 ± 0.9). Tear production returned to normal (4.3 ± 0.7 mm/10s) at day 7 post IL–1α injection. IL–1α induced a severe inflammatory response in the lacrimal gland that subsided by day 7. At day 1 following injection of IL–1α, Ki67 staining was detected in the infiltrating immune cells. Two and 3 days following IL–1α injection, Ki67 immunoreactivity was seen in acinar and ductal cells, and this subsided at day 7. KCl–induced protein secretion was inhibited by 91%, 67%, and 33% at 1–, 2–, and 3–day post IL–1α injection, respectively. Phenylephrine– and carbachol–induced protein secretion was similarly inhibited. Both KCl– and agonist–induced protein secretions returned to normal at 7–days post IL–1α injection. Similar results were obtained in C57BL/6 mice.
A single injection of IL–1α into the lacrimal gland inhibited neurally– as well as agonist–induced protein secretion resulting in decreased tear output, induced a severe but reversible inflammatory response, and stimulated cell proliferation.
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