scholarly journals Lactobacillus acidophilusSuppresses Colitis-Associated Activation of the IL-23/Th17 Axis

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Linlin Chen ◽  
Yiyou Zou ◽  
Jie Peng ◽  
Fanggen Lu ◽  
Yani Yin ◽  
...  
Keyword(s):  
Lactobacillus Acidophilus ◽  
Proinflammatory Cytokine ◽  
Th17 Cell ◽  
Transforming Growth Factor ◽  
Immunohistochemical Analysis ◽  
Experimental Colitis ◽  
Signal Transducer ◽  
Rt Pcr ◽  
Transcription 3 ◽  
Necrosis Factor

The aim of this paper is to determine the modulatory effects ofLactobacillus acidophiluson the IL-23/Th17 immune axis in experimental colitis. DSS-induced mouse models of UC were to be saline, hormones, and different concentrations ofLactobacillus acidophilusintervention. The expression of interleukin- (IL-) 17, tumor necrosis factorα(TNFα), IL-23, transforming growth factorβ1 (TGFβ1), signal transducer and activator of transcription 3 (STAT3), and phosphorylated (p)-STAT3 was examined by RT-PCR, Western blotting, and immunohistochemical analysis. And the results showed that administration ofL. acidophilussuppressed Th17 cell-mediated secretion of proinflammatory cytokine IL-17 through downregulation of IL-23 and TGFβ1 expression and downstream phosphorylation of p-STAT3.

scholarly journals Adrenal Corticomedullary Mixed Tumor Associated With the FGFR4-G388R Variant

2020 ◽  
Vol 4 (9) ◽  
Author(s):  
Maki Kanzawa ◽  
Hidenori Fukuoka ◽  
Akane Yamamoto ◽  
Kentaro Suda ◽  
Katsumi Shigemura ◽  
...  
Keyword(s):  
Gestational Hypertension ◽  
Immunohistochemical Analysis ◽  
Serine Phosphorylation ◽  
Adrenocortical Adenoma ◽  
Signal Transducer ◽  
Double Immunostaining ◽  
Psychiatric Disturbances ◽  
Peripheral Leukocytes ◽  
Transcription 3 ◽  
Mixed Tumors

Abstract Adrenal corticomedullary mixed tumors (CMMTs) are extremely rare; with only 20 cases being reported to date, the pathogenesis has remained elusive. A 31-year-old woman developed gestational hypertension with psychiatric disturbances persistent to postpartum and was diagnosed with pheochromocytoma, for which adrenalectomy was performed. Histological findings showed mixed adrenocortical adenoma and pheochromocytoma. Double immunostaining of inhibin and INSM1 (insulinoma-associated protein 1) showed that the 2 tumor components had distinct functional properties. Exome analysis of peripheral leukocytes and tumor (singular, as anatomically it is only 1 mass) revealed a homozygous germline FGFR4-G388R variant. As a readout of the variant, serine phosphorylation of signal transducer and activator of transcription 3 (STAT3) was detected only in the nucleus of adrenocortical adenoma component but not in the pheochromocytoma component. No tyrosine phosphorylation of STAT3 was detected. We report a case of CMMT with the germline FGFR4-G388R variant. Although additional studies are required, our immunohistochemical analysis suggests that the variant may play a role in the development of the adrenocortical component within the pheochromocytoma, leading to CMMT.

scholarly journals Cloning of porcine signal transducer and activator of transcription 3 cDNA and its expression in reproductive tissues

Reproduction ◽  
2006 ◽  
Vol 132 (3) ◽  
pp. 511-518 ◽  
Author(s):  
Lihua Wen ◽  
Jesse Craig ◽  
Paul W Dyce ◽  
Julang Li
Keyword(s):  
Growth Factor ◽  
Ovarian Function ◽  
Control Level ◽  
Signal Transducer ◽  
Rt Pcr ◽  
Western Blots ◽  
Epidermal Growth ◽  
Mucosal Folds ◽  
Transcription 3 ◽  
Phosphorylated Stat3

The signal transducer and activator of transcription 3 (Stat3) protein is a member of the Stat family that has a variety of biological functions including cell growth, anti-apoptosis, and cell motility, depending on the cell type and stimulus. Recent studies have suggested that Stat3 plays an important role in embryo development. Although the Stat3 gene has been cloned in humans, mice, cow, and rats, its sequence in pigs is unknown. In the present study, the 2476 bp Stat3 cDNA was cloned using real time reverse transcriptase (RT)-PCR. Comparison of sequences across species revealed that the porcine Stat3 cDNA is 93 and 90% homologous to human and mouse respectively. To study the expression pattern of Stat3, RNA and protein were isolated from heart, lung, kidney, ovary, oviduct, and uterus tissues. RT-PCR and western blot indicated that Stat3 is expressed in all the tissues tested, and the level of expression is relatively high in tissues from the reproductive system. In addition, immunohistochemistry studies suggested that the Stat3 protein was present in the oocyte, granulosa, theca, and interstitial cells of the ovary, the mucosal folds in the oviduct, and both the epithelium and stromal layers in the endometrium. To study whether Stat3 is functional in responding to growth factor stimulation in the ovary, granulosa cells were isolated from large follicles (>3 mm) and cultured in the presence of epidermal growth factor (EGF; 10 ng/ml) for 5, 10, 15, 30, and 60 min, following which western blots were performed using an antibody against the phosphorylated Stat3. Phosphorylated Stat3 was upregulated following 5 min of EGF challenge and was sustained during the 15-min stimulation, and decreased back to the control level following 60-min stimulation. The translocation of phosphorylated Stat3 from cytoplasm to nucleus following stimulation of EGF was also detected via immunocytochemistry. Our data suggests that Stat3 may play a role in porcine ovarian function.

scholarly journals Divergent Leptin Signaling in Proglucagon Neurons of the Nucleus of the Solitary Tract in Mice and Rats

Endocrinology ◽  
2007 ◽  
Vol 149 (2) ◽  
pp. 492-497 ◽  
Author(s):  
Lihong Huo ◽  
Kevin M. Gamber ◽  
Harvey J. Grill ◽  
Christian Bjørbæk
Keyword(s):  
Species Differences ◽  
Signal Transducer ◽  
Solitary Tract ◽  
Rt Pcr ◽  
Mechanism Of Interaction ◽  
The Central Nervous System ◽  
Ad Libitum ◽  
Glucagon Like Peptide ◽  
Transcription 3 ◽  
Striking Contrast

The central targets mediating the anorectic and other actions of leptin have yet to be fully identified. Although previous studies focused on the hypothalamus, leptin also acts on neurons in extrahypothalamic sites, including the nucleus of the solitary tract (NTS). Moreover, injection of leptin into the NTS of rats suppresses food intake. Within the central nervous system, glucagon-like peptide (GLP-1), a product of proglucagon, is synthesized almost exclusively in neurons of the NTS. Intracerebroventricular administration of GLP-1 inhibits energy intake, and GLP-1 receptor antagonists attenuate the anorexic effects of leptin in rats. To examine whether NTS proglucagon neurons are directly regulated by leptin, we performed double GLP-1 and phosphorylation of signal transducer and activator of transcription-3 immunohistochemistry on brain sections from ip leptin-treated mice and rats. Leptin induced phosphorylation of signal transducer and activator of transcription-3 in 100% of GLP-1 cells in the caudal brainstem of mice. In striking contrast, 0% of GLP-1-positive neurons in rats responded to leptin. We then measured regulation of NTS proglucagon mRNA using real-time RT-PCR in mice and rats fed ad libitum, fasted, or fasted and treated ip with leptin. In mice, proglucagon mRNA fell by fasting, and this was prevented by leptin administration. In rats, by contrast, proglucagon mRNA was unaffected by either fasting or leptin. Taken together, our studies reveal direct regulation of proglucagon neurons by leptin in mice but not rats along with corresponding species differences in the regulation of proglucagon mRNA expression. These data, combined with previous results, suggest a different mechanism of interaction between leptin and NTS proglucagon neurons in mice and rats.

scholarly journals Low-Dose UVB Contributes to Host Resistance against Leishmania amazonensis Infection in Mice through Induction of Gamma Interferon and Tumor Necrosis Factor Alpha Cytokines

2002 ◽  
Vol 9 (3) ◽  
pp. 677-686 ◽  
Author(s):  
Noor Mohammad Khaskhely ◽  
Motoyoshi Maruno ◽  
Hiroshi Uezato ◽  
Atsushi Takamiyagi ◽  
Saeef Taher Ramzi ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Low Dose ◽  
Immunohistochemical Analysis ◽  
Rt Pcr ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Ifn Γ ◽  
Necrosis Factor

ABSTRACT UV radiation suppresses the immune response, a fact which raises the question of whether the phenomenon may find practical applications in the outcome of infectious diseases. In this study, BALB/c mice were exposed to low-dose UVB (250 J/m2) from Dermaray M-DMR-100 for 4 consecutive days. Twelve hours after the last UV exposure, groups of mice were injected with 2 × 106 Leishmania amazonensis promastigotes. The development of skin lesions, as assessed by measurement of visible cutaneous lesions, was significantly suppressed in low-dose UVB-irradiated mice compared to nonirradiated controls. In order to characterize the cytokines involved in this phenomenon, BALB/c mice were irradiated with identical doses of UVB, and gamma interferon (IFN-γ), tumor necrosis factor alpha (TNF-α), and interleukin 4 cytokine levels in blood serum and skin were examined at different times by a sandwich enzyme-linked immunosorbent assay, immunohistochemical analysis, and reverse transcription (RT)-PCR. Upregulated expression of serum IFN-γ and TNF-α was observed from 6 to 24 h. Positive results for IFN-γ and TNF-α in UVB-irradiated mice were obtained by immunohistochemical analysis. By RT-PCR, the mRNA expression of both IFN-γ and TNF-α cytokines was detected in a time-dependent manner only in UVB-irradiated mice. Histopathological analysis and electron microscopy revealed that cellular infiltration, tissue parasitism, and parasitophorus vacuoles in irradiated mice were markedly less noticeable than those in nonirradiated controls. These results suggested that low-dose UVB irradiation played a pathogen-suppressing role in Leishmania-susceptible BALB/c mice via systemic and local upregulation of Th1 (IFN-γ and TNF-α) cytokines.

scholarly journals Microglia Stimulate Zebrafish Brain Repair Via a Specific Inflammatory Cascade

2020 ◽  
Author(s):  
Palsamy Kanagaraj ◽  
Jessica Y. Chen ◽  
Kaia Skaggs ◽  
Yusuf Qadeer ◽  
Meghan Conner ◽  
...  
Keyword(s):  
Progenitor Cell ◽  
Mammalian Brain ◽  
Signal Transducer ◽  
Brain Repair ◽  
Zebrafish Brain ◽  
Ectopic Activation ◽  
Factor Α ◽  
Transcription 3 ◽  
Stimulating Factor ◽  
Necrosis Factor

AbstractThe adult zebrafish brain, unlike mammals, has a remarkable regenerative capacity. Although inflammation inhibits regeneration in mammals, it is necessary for zebrafish brain repair. Microglia are resident brain immune cells that regulate the inflammatory response. To explore the microglial role in repair, we used liposomal clodronate and colony stimulating factor-1 receptor (csf1r) inhibition to suppress microglia during brain injury. We found that microglial ablation inhibited injury-induced neurogenesis and regeneration. Microglial suppression specifically attenuated cell proliferation at the progenitor cell amplification stage of neurogenesis. Notably, the loss of microglia impaired phospho-stat3 (signal transducer and activator of transcription 3) and ß-catenin signaling by altering tumor necrosis factor-α expression after injury, and the ectopic activation of stat3 and ß-catenin rescued neurogenesis defects caused by microglial loss. Leukocytes also accumulated after microglial ablation, potentially hindering the resolution of inflammation. These findings reveal specific roles of microglia and inflammatory signaling during zebrafish telencephalic regeneration that should provide strategies to improve mammalian brain repair.

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