Lacrimal gland fluid secretion and lymphocytic infiltration in the NZB/W mouse model of Sjogren's syndrome

被引:13
|
作者
Paranyuk, Y
Claros, N
Birzgalis, A
Moore, LC
Brink, PR
Walcott, B [1 ]
机构
[1] SUNY Stony Brook, Sch Med, Dept Neurobiol & Behav, Stony Brook, NY 11794 USA
[2] SUNY Stony Brook, Sch Med, Dept Physiol & Biophys, Stony Brook, NY 11794 USA
关键词
carbachol; tear flow; dry-eye syndrome; protein secretion; autoimmune disease;
D O I
10.1076/ceyr.23.3.199.5468
中图分类号
R77 [眼科学];
学科分类号
100212 ;
摘要
Purpose. The fluid secretory impairment of lacrimal and salivary glands in Sjogren's syndrome (SS) is thought to be related to the extent of lymphocytic infiltration (LI) and subsequent loss of glandular tissue. In this study, we examine the correlation between the extent of tear flow reduction and the extent of LI of lacrimal glands in the NZB/W mouse, a model of SS. Methods. We stimulated tear production by topical application of carbachol onto the gland while fluid was collected from the lacrimal duct. The lacrimal glands were removed after fluid collection for histology. Results. Fluid secretion in response to carbachol was less in the majority of young NZB/W females compared to C57 control animals and none of the glands showed LI. Fluid secretion was also impaired in the majority of old NZB/W females, and the extent of LI was highly variable. Some of the old SW females also showed blunted fluid secretory responses and some degree of focal LI. Young SW females showed no LI and most animals exhibited normal flow responses. Analysis of paired flow and LI measurements showed no correlation between LI and flow impairment in any of the groups or in the pooled data. Carbachol-stimulated protein secretion from lacrimal gland slices in vitro were similar in young and old SW and NZB/W mice. Conclusions. These results suggest that LI alone is not sufficient to explain the secretory dysfunction in the NZB/W mouse model of Sjogren's syndrome.
引用
收藏
页码:199 / 205
页数:7
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