Reduced Thymic Size and Numbers of Splenic CD4<sup>+</sup>and CD8<sup>+</sup>Cells in Artificially Reared Mouse Pups

Yajima, Motoyuki; Hoshiba, Junji; Terahara, Masaki; Yajima, Takaji

doi:10.1271/bbb.70121

Cited by 14 publications

(18 citation statements)

References 30 publications

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“…Neonatal mice delivered via cesarean section were fed~20 mg of milk every 3 h. Hand-feeding of formula milk with a nursing bottle of Hoshiba Nipple-Yajima Style (provided by Meiji Dairies Corporation) was done as described. 26,27) Histology and immunohistochemistry. Immunohistochemistry was done essentially as described.…”

Section: Methodsmentioning

confidence: 99%

Activating transcription factor 5 is required for mouse olfactory bulb development via interneuron

Umemura

Tsunematsu

Shimizu

et al. 2015

Bioscience, Biotechnology, and Biochemistry

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Activating transcription factor 5 (ATF5) is a stress response transcription factor of the cAMP-responsive element-binding/ATF family. Earlier, we reported that ATF5 expression is up-regulated in response to stress, such as amino acid limitation or arsenite exposure. Although ATF5 is widely expressed in the brain and the olfactory epithelium, the role of ATF5 is not fully understood. Here, the olfactory bulbs (OBs) of ATF5-deficient mice are smaller than those of wild-type mice. Histological analysis reveals the disturbed laminar structure of the OB, showing the thinner olfactory nerve layer, and a reduced number of interneurons. This is mainly due to the reduced number of bromodeoxyuridine-positive proliferating cells in the subventricular zone, where the interneuron progenitors are formed and migrate to the OBs. Moreover, the olfaction-related aggressive behavior of ATF5-deficient mice is reduced compared to wild-type mice. Our data suggest that ATF5 plays a crucial role in mouse OB development via interneuron.

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Section: Methodsmentioning

confidence: 99%

Activating transcription factor 5 is required for mouse olfactory bulb development via interneuron

Umemura

Tsunematsu

Shimizu

et al. 2015

Bioscience, Biotechnology, and Biochemistry

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“…BSEP-overexpressing mice (C57BL/6 TTRAbcb11; BSEP OE) were kindly provided by Dr. Richard M. Green (Northwestern University, Evanston, IL) (13,23). Each strain was divided into two groups: one containing pups that were dam-fed [ASBT WT DF (n ϭ 10), ASBT KO DF (n ϭ 10), BSEP WT DF (n ϭ 10), and BSEP OE DF (n ϭ 10)] and the other consisting of pups subjected to the NEC protocol, i.e., newborn mice collected immediately after birth to prevent suckling of maternal milk and hand-fed a cow's milk-based formula using the Hoshiba nipple [Yajima style (25,45); Meiji Dairies, Tokyo, Japan] every 2-3 h for up to 3 days [ASBT WT NEC (n ϭ 16), ASBT KO NEC (n ϭ 24), BSEP WT NEC (n ϭ 25), and BSEP OE NEC (n ϭ 21)]. All pups from the DF and NEC groups were subjected to A/C stress twice daily (18).…”

Section: Methodsmentioning

confidence: 99%

Apical sodium-dependent bile acid transporter upregulation is associated with necrotizing enterocolitis

Halpern

Weitkamp²,

Patrick

et al. 2010

American Journal of Physiology-Gastrointestinal and Liver Physi

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Necrotizing enterocolitis (NEC) is the most common gastrointestinal emergency of premature infants. Previously, we showed that luminal bile acids (BAs) are increased and correlated with disease development and that the apical sodium-dependent BA transporter (ASBT), which transports BAs from the ileal lumen into enterocytes, is upregulated in rats with NEC. We hypothesized that intraenterocyte, rather than luminal, BAs are associated with NEC and that upregulation of ASBT may be a mechanism by which this occurs. Neonatal rats with or without the ASBT inhibitor SC-435, mice in which ASBT was knocked out, and mice that overproduce BAs were subjected to the NEC protocol. Disease development, ASBT, and the farnesoid X receptor protein, along with luminal and intraenterocyte BA levels, were assessed. In addition, ileal sections from premature infants with and without NEC were examined for ASBT via immunohistology and real-time PCR. When BAs were not transported into enterocytes (rats given SC-435 and ASBT knockout mice), severity and incidence of NEC were reduced. In contrast, in mice that overproduce BAs, ASBT was elevated, intraenterocyte BAs were increased, and disease development was increased. ASBT staining was more intense on the apical membrane of ileal enterocytes from premature infants with NEC than premature infants with non-NEC diagnoses. In addition, ASBT mRNA levels were significantly higher in infants with NEC. These data show that accumulation of intraenterocyte BAs contributes to disease development, elevated ASBT increases disease severity in experimental models of NEC, and ASBT is elevated in human NEC. These data confirm that BAs and upregulation of ASBT play a crucial role in NEC pathogenesis and suggest that inhibition of ASBT could be utilized as a therapeutic modality against this disease.

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“…Newborn IL-18 Ϫ/Ϫ (NEC IL-18 Ϫ/Ϫ ) and WT (NEC WT) mice were collected immediately after birth to prevent suckling of maternal milk. All pups were hand fed 50 l of rat milk substitute every 3 h for 3 days using the Hoshiba nipple, Yajima style (19,44) developed and manufactured by Meiji Dairies (Tokyo, Japan). With the use of this device ( Fig.…”

Section: Methodsmentioning

confidence: 99%

Decreased development of necrotizing enterocolitis in IL-18-deficient mice

Halpern

Khailová

Molla-Hosseini

et al. 2008

American Journal of Physiology-Gastrointestinal and Liver Physi

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Necrotizing enterocolitis (NEC) is a devastating gastrointestinal disease predominantly of prematurely born infants, characterized in its severest from by extensive hemorrhagic inflammatory necrosis of the distal ileum and proximal colon. Proinflammatory cytokines have been implicated in the development of NEC, and we have previously shown that IL-18 is significantly elevated in the well-established neonatal rat model of NEC. To determine whether IL-18 contributes to intestinal pathology in NEC, we subjected IL-18 knockout mice to the protocol used to develop experimental NEC in newborn rats. Newborn B6.129P2-Il18(tm1Aki)/J (NEC IL-18(-/-)) and wild-type (NEC WT) mice were hand fed every 3 h with cow's milk-based formula and exposed to asphyxia and cold stress twice daily. After 72 h, animals were killed and distal ileum and liver were removed. Disease development was determined via histological changes in the ileum as scored by a blinded evaluator. The number of TNF-alpha-, IL-12-, and IL-1beta-positive cells and macrophages were determined in both ileum and liver via immunohistology. IkappaB-alpha and IkappaB-beta were determined from protein extracts from both ileum and liver using Western blot analysis. The incidence and severity of NEC was significantly reduced in NEC IL-18(-/-) mice compared with NEC WT. Furthermore, mean ileal macrophages and hepatic IL-1beta were significantly reduced in IL-18(-/-) mice subjected to the NEC protocol. There were no statistically significant changes in Kupffer cells, hepatic TNF-alpha, ileal IL-1beta, or IL-12. IkappaB-alpha and IkappaB-beta were significantly increased in NEC IL-18(-/-) mice ileum and liver, respectively. These results confirm that IL-18 plays a crucial role in experimental NEC pathogenesis.

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Reduced Thymic Size and Numbers of Splenic CD4⁺and CD8⁺Cells in Artificially Reared Mouse Pups

Cited by 14 publications

References 30 publications

Activating transcription factor 5 is required for mouse olfactory bulb development via interneuron

Activating transcription factor 5 is required for mouse olfactory bulb development via interneuron

Apical sodium-dependent bile acid transporter upregulation is associated with necrotizing enterocolitis

Decreased development of necrotizing enterocolitis in IL-18-deficient mice

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Reduced Thymic Size and Numbers of Splenic CD4+and CD8+Cells in Artificially Reared Mouse Pups

Cited by 14 publications

References 30 publications

Activating transcription factor 5 is required for mouse olfactory bulb development via interneuron

Activating transcription factor 5 is required for mouse olfactory bulb development via interneuron

Apical sodium-dependent bile acid transporter upregulation is associated with necrotizing enterocolitis

Decreased development of necrotizing enterocolitis in IL-18-deficient mice

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Reduced Thymic Size and Numbers of Splenic CD4⁺and CD8⁺Cells in Artificially Reared Mouse Pups