Effect of cholecystokinin receptor blockade on human lymphocyte proliferation

Ferrara, Andrea; McMillen, Marvin A.; Schaefer, H. C.; Zucker, Karl A.; Modlin, Irvin M.

doi:10.1016/0022-4804(90)90074-c

Cited by 13 publications

(1 citation statement)

References 16 publications

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“…Several cell types of the immune system express CCK and both of its receptors (Sacerdote et al ., 1991; Cuq et al ., 1997). In addition, CCK, through its receptors has been shown to modulate mobility and mitogenesis of monocytes and lymphocytes (Ferrara et al ., 1990; Tang et al ., 1992; De la Fuente et al ., 1998) and thus modifies development of inflammation (de la Mano et al ., 2004; Ribot et al ., 2003). Therefore, we can speculate that in CCK 2 receptor mutant mice, inflammatory response is badly localized.…”

Section: Discussionmentioning

confidence: 99%

Deletion of the CCK₂ receptor gene reduces mechanical sensitivity and abolishes the development of hyperalgesia in mononeuropathic mice

Kurrikoff

Kõks

Matsui

et al. 2004

Eur J of Neuroscience

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Previous studies suggest that cholecystokinin (CCK) is implicated in the modulation of pain sensitivity and the development of neuropathic pain. We used CCK(2) receptor deficient (CCK(2) (-/-)) mice and assessed their mechanical sensitivity using Von Frey filaments, as well as the development and time course of mechanical hyperalgesia in a model of neuropathic pain. We found that CCK(2) (-/-) mice displayed mechanical hyposensitivity, which was reversed to the level of wild-type animals after administration of naloxone (0.1-10 mg/kg). On the other hand, injection of L-365260 (0.01-1 mg/kg), an antagonist of CCK(2) receptors, decreased dose-dependently, mechanical sensitivity in wild-type mice. The mechanism of reduced mechanical sensitivity in CCK(2) (-/-) mice may be explained by changes in interactions between CCK and opioid systems. Indeed, CCK(2) (-/-) mice natively expressed higher levels of lumbar CCK(1), opioid delta and kappa receptors. Next, we found that CCK(2) (-/-) mice did not develop mechanical hyperalgesia in the Bennett's neuropathic pain model. Induction of neuropathy resulted in decrease of lumbar pro-opiomelanocortin (POMC) gene expression in wild-type mice, but increase of POMC expression in CCK(2) (-/-) mice. In addition, induction of neuropathy resulted in further increase of opioid delta receptor in CCK(2) (-/-) mice. Gene expression results indicate up-regulation of opioid system in CCK(2) (-/-) mice, which apparently result in decreased neuropathy score. Our study suggests that not only pain sensitivity, but also mechanical sensitivity and the development of neuropathic pain are regulated by antagonistic interactions between CCK and opioid systems.

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Section: Discussionmentioning

confidence: 99%

Deletion of the CCK₂ receptor gene reduces mechanical sensitivity and abolishes the development of hyperalgesia in mononeuropathic mice

Kurrikoff

Kõks

Matsui

et al. 2004

Eur J of Neuroscience

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Cellular and Molecular Targets of Gastrin

Tarasova¹

1999

Gastrointestinal Endocrinology

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Effects of CCK-8 and CCK-33 on human natural killer cell activity: studies on intestinal lamina propria and peripheral blood mononuclear cells

Tol¹,

Verspaget²,

Lamers³

1993

Immunopharmacology

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Effect of cholecystokinin receptor blockade on human lymphocyte proliferation

Cited by 13 publications

References 16 publications

Deletion of the CCK₂ receptor gene reduces mechanical sensitivity and abolishes the development of hyperalgesia in mononeuropathic mice

Deletion of the CCK₂ receptor gene reduces mechanical sensitivity and abolishes the development of hyperalgesia in mononeuropathic mice

Cellular and Molecular Targets of Gastrin

Effects of CCK-8 and CCK-33 on human natural killer cell activity: studies on intestinal lamina propria and peripheral blood mononuclear cells

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Effect of cholecystokinin receptor blockade on human lymphocyte proliferation

Cited by 13 publications

References 16 publications

Deletion of the CCK2 receptor gene reduces mechanical sensitivity and abolishes the development of hyperalgesia in mononeuropathic mice

Deletion of the CCK2 receptor gene reduces mechanical sensitivity and abolishes the development of hyperalgesia in mononeuropathic mice

Cellular and Molecular Targets of Gastrin

Effects of CCK-8 and CCK-33 on human natural killer cell activity: studies on intestinal lamina propria and peripheral blood mononuclear cells

Contact Info

Product

Resources

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Deletion of the CCK₂ receptor gene reduces mechanical sensitivity and abolishes the development of hyperalgesia in mononeuropathic mice

Deletion of the CCK₂ receptor gene reduces mechanical sensitivity and abolishes the development of hyperalgesia in mononeuropathic mice