Gastrin/cholecystokinin-like immunoreactivity in human blood cells

Okahata, Hiroyasu; Nishi, Yoshikazu; Muraki, Kotaro; Sumii, Koji; Miyachi, Yukitaka; Usui, Tateo

doi:10.1016/0024-3205(85)90123-7

Cited by 13 publications

(6 citation statements)

References 6 publications

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“…Cholecystokinin immunoreactivity has consistently been found to be expressed in human and rat mononuclear cells in blood (106, 107). Moreover, CCK-8 (sulfated as well as non-sulfated) has been reported to exert a wide specter of stimulation and inhibition on lymphocytes, macrophages, and cytokine release, with ensuing anti-inflammatory effects (108–111).…”

Section: Novel Sites Of Expressionmentioning

confidence: 99%

Cholecystokinin—From Local Gut Hormone to Ubiquitous Messenger

2017

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Cholecystokinin (CCK) was discovered in 1928 in jejunal extracts as a gallbladder contraction factor. It was later shown to be member of a peptide family, which are all ligands for the CCK1 and CCK2 receptors. CCK peptides are known to be synthetized in small intestinal endocrine I-cells and cerebral neurons. But in addition, CCK is expressed in several endocrine glands (pituitary cells, thyroid C-cells, pancreatic islets, the adrenals, and the testes); in peripheral nerves; in cortical and medullary kidney cells; in cardial myocytes; and in cells of the immune system. CCK peptides stimulate pancreatic enzyme secretion and growth, gallbladder contraction, and gut motility, satiety and inhibit acid secretion from the stomach. Moreover, they are major neurotransmitters in the brain and the periphery. CCK peptides also stimulate calcitonin, insulin, and glucagon secretion, and they may act as natriuretic peptides in the kidneys. CCK peptides are derived from proCCK with a C-terminal bioactive YMGWMDFamide sequence, in which the Y-residue is partly O-sulfated. The plasma forms are CCK-58, -33, -22, and -8, whereas the small CCK-8 and -5 are potent neurotransmitters. Over the last decades, CCK expression has also been encountered in tumors (neuroendocrine tumors, cerebral astrocytomas, gliomas, acoustic neuromas, and specific pediatric tumors). Recently, a metastastic islet cell tumor was found to cause a specific CCKoma syndrome, suggesting that circulating CCK may be a useful tumor marker.

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Section: Novel Sites Of Expressionmentioning

confidence: 99%

Cholecystokinin—From Local Gut Hormone to Ubiquitous Messenger

2017

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Section: Discussionmentioning

confidence: 72%

“…Cholecystokinin is released from specialized enteroendocrine cells of the upper small intestine and stimulates NTS neurons, the primary site of synapses of vagal afferents that transmit mealrelated satiety signals from the gastrointestinal system (Dockray, 2009). In addition, CCK expression was also reported in leucocytes (Okahata et al 1985). Therefore, CCK released from peripheral sources and also in the hypothalamus might contribute to the effects of this peptide on neuroendocrine and behavioural responses during endotoxaemia.…”

Section: Representative Photomicrographs Of Coronal Sections Of Nts mentioning

confidence: 93%

Cholecystokinin and hypothalamic corticotrophin-releasing factor participate in endotoxin-induced hypophagia

Rorato

Reis

Antunes‐Rodrigues

et al. 2011

Experimental Physiology

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“…The first evidence of a relationship between gastrin and immune system was reported by Okahata et al [14], who demonstrated gastrin immunoreactivity in pure populations of polymorphonuclear leukocytes and mononuclear cells from human peripheral blood. Gastrin is a negative modulator of the phagocytosis by human neutrophils, suppresses their apoptosis and increases chemotaxis [15].…”

Section: Discussionmentioning

confidence: 98%

Serum gastrin concentration in neonates with early-onset severe infections

Stojewska¹,

Oświęcimska²,

Stachurska³

et al. 2017

Pediatr. Endocrinol.

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Słowa kluczowe gastryna, noworodek donoszony, noworodek urodzony przedwcześnie, wczesne zakażenie Streszczenie Wstęp. Wpływ wczesnych zakażeń na stężenie gastryny u noworodków nie został dobrze poznany. Cel. Ocena stężeń gastryny w surowicy u noworodków z uwzględnieniem ich płci, dojrzałości ciążowej, sposobu urodzenia, wystąpienia wczesnego zakażenia, niedotlenienia i zaburzeń przewodu pokarmowego. Materiał i metody. U 97 (54 donoszonych, 43 urodzonych przedwcześnie) noworodków, w tym u 54 z zakażeniami i 43 zdrowych, oznaczono dwukrotnie metodą radioimmunologiczną stężenie gastryny. Wyniki. W pierwszym tygodniu życia noworodki donoszone z zakażeniem miały istotnie statystycznie wyższe wartości gastryny niż zdrowe i urodzone przedwcześnie z zakażeniem. W trzecim tygodniu życia wcześniaki z zakażeniem miały istotnie wyższe wartości gastryny niż zdrowe i wyższe niż chore noworodki donoszone. Wykazano niższe stężenia gastryny u noworodków donoszonych z zakażeniem i zaburzeniami przewodu pokarmowego niż u noworodków z zakażeniem bez tych objawów. Wcześniactwo i wczesne zakażenia okazały się niezależnymi czynnikami predykcyjnymi stężeń gastryny w obu pomiarach. Wnioski. 1. Róż-nice w stężeniu gastryny w surowicy między noworodkami donoszonymi i urodzonymi przedwcześnie mogą zależeć od wystąpienie wczesnych ciężkich zakażeń wymagających intensywnej terapii, od dojrzałości i zaburzeń czynnościowych przewodu pokarmowego Key words gastrin, full-term neonate, preterm neonate, earlyonset infection Abstract Introduction. Effect of early-onset infections on serum gastrin concentration in neonates is not well known. Aim. The evaluation of serum gastrin concentration in neonates with regards to their sex, fetal maturity, type of delivery, occurrence of early-onset infections, birth asphyxia and gastrointestinal disorders. Material and methods. In 97 (54 full-term, 43 preterm) neonates, among them 54 infected and 43 healthy ones, twice serum gastrin concentration by radioimmunoassay was measured. Results. Infected full-term neonates in the first week of life had significantly higher gastrin concentration than infected preterm neonates and healthy full-term. In the third week of life, infected preterm neonates had higher mean gastrin value than healthy preterm and infected full--term neonates. Significant lower mean gastrin concentration was noted in infected full-term neonates with gastrointestinal disorders than in infected neonates without these signs. Prematurity and presence of early-onset infection in neonates were independent predictors of gastrin values in both measurements. Conclusions. 1. Differences in serum gastrin concentrations between full-term and preterm neonates may depend on early-onset severe infections connected with intensive therapy, on gastrointestinal tract maturity and functional disorders and type of nutrition. 2. Higher gastrin concentrations in infected full-term

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Gastrin/cholecystokinin-like immunoreactivity in human blood cells

Cited by 13 publications

References 6 publications

Cholecystokinin—From Local Gut Hormone to Ubiquitous Messenger

Cholecystokinin—From Local Gut Hormone to Ubiquitous Messenger

Cholecystokinin and hypothalamic corticotrophin-releasing factor participate in endotoxin-induced hypophagia

Serum gastrin concentration in neonates with early-onset severe infections

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