Immunohistopathology of Sjögren's syndrome

Konttinen, Yrjö T.; Porola, Pauliina; Konttinen, Liisa; Laine, Mikael; Poduval, Praseet

doi:10.1016/j.autrev.2006.03.003

Cited by 38 publications

(25 citation statements)

References 10 publications

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“…Instead, histamine may be released from the salivary gland itself and act in an autocrine manner. Acetylcholine is secreted from parasympathetic terminals and diffuses approximately 100 nm before stimulating receptors on the salivary acinar cell membrane (Konttinen et al, 2006). Sympathetic neurons, with limited axon terminals to modulate a target organ, possess varicosities to increase the number of synaptic contacts (Konttinen et al, 1996); however, such varicosities are relatively less developed in parasympathetic neurons (Arvidsson et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

Histamine H1 Receptor Induces Cytosolic Calcium Increase and Aquaporin Translocation in Human Salivary Gland Cells

Kim¹,

Park²,

Moon³

et al. 2009

J Pharmacol Exp Ther

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One of the common side effects of antihistamine medicines is xerostomia (dry mouth). The current consensus is that antihistamine-induced xerostomia comes from an antimuscarinic effect. Although the effect of antihistamines on salivary secretion is both obvious and significant, the cellular mechanism whereby this happens is still unclear because of the lack of knowledge of histamine signaling in human salivary glands. Here, we have studied histamine receptors and the effect of antihistamines on human submandibular acinar cells. In primary cultured human submandibular gland and a HSG cell line, histamine increased the intracellular Ca 2ϩ concentration. The histamine-induced cytosolic free Ca 2ϩ concentration ([Ca 2ϩ ] i ) increase was inhibited by histamine H1 receptor-specific antagonists, and the expression of the functional histamine H1 receptor was confirmed by reverse transcription-polymerase chain reaction. Interestingly, histamine pretreatment did not inhibit a subsequent carbachol-induced [Ca 2ϩ ] i rise without "heterologous desensitization." Chlorpheniramine inhibited a carbachol-induced [Ca 2ϩ ] i increase at a 100-fold greater concentration than histamine receptor antagonism, whereas astemizole and cetrizine showed more than 1000-fold difference, which in part explains the xerostomia-inducing potency among the antihistamines. Notably, histamine resulted in translocation of aquaporin-5 to the plasma membrane in human submandibular gland cells and green fluorescent proteintagged aquaporin-5 expressing HSG cells. We found that histidine decarboxylase and the histamine H1 receptor are broadly distributed in submandibular gland cells, whereas choline acetyltransferase is localized only at the parasympathetic terminals. Our results suggest that human salivary gland cells express histamine H1 receptors and histamine-synthesizing enzymes, revealing the cellular mechanism of antihistamineinduced xerostomia.

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Section: Discussionmentioning

confidence: 99%

Histamine H1 Receptor Induces Cytosolic Calcium Increase and Aquaporin Translocation in Human Salivary Gland Cells

Kim¹,

Park²,

Moon³

et al. 2009

J Pharmacol Exp Ther

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“…It is not known how much various cells take up DHEA or other pro-hormones or to what extent these pro-hormones taken into the cells are converted to estrogens and androgens or something else of (patho) biological relevance. To be able to better assess this, we are trying to use biomarkers, as described in some detail elsewhere [20]. Some are in part estrogen-regulated, namely solute carrier family 39, member 6 (SLC39A6, also known as leucin-isoleucine-valine transporter, LIV-1) and cystein-rich, angiogenic inducer, 61 (CYR61, also known as insulin-like growth factor binding protein 10, IGFBP-10).…”

Section: Local Intracrine Aspects In Healthy Individualsmentioning

confidence: 99%

Sex steroids in Sjögren’s syndrome

Konttinen

Fuellen

Yan

et al. 2012

Journal of Autoimmunity

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“…It has been proposed that a loss of homeostatic equilibrium in the glands is partly responsible for salivary dysfunction which would, in turn, increase the susceptibility of the glands to the autoimmune attack [3][4][5][6]. In line with this, labial biopsies and acinar cell primary cultures from SS patients show an aberrant expression and activation of inflammatory mediators in epithelial cells together with defective activity and localization of key enzymes and channels involved in saliva secretion [5][6][7][8]. This observation supports the hypothesis that acinar cells are involved actively in the pathogenesis of SS and provides new evidence to the search of early biomarkers for diagnosis and/or disease activity.…”

Section: Introductionmentioning

confidence: 99%