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Filename: drivers/Session_files_driver.php
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Function: require_once
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File: /var/www/html/index.php
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Function: require_once
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Filename: controllers/Detail.php
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Line: 249
Function: _error_handler
File: /var/www/html/index.php
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Function: require_once
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Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
Line: 249
Function: _error_handler
File: /var/www/html/index.php
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Message: Trying to access array offset on value of type null
Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
Line: 249
Function: _error_handler
File: /var/www/html/index.php
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Function: require_once
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Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
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Function: _error_handler
File: /var/www/html/index.php
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Filename: models/Detail_model.php
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File: /var/www/html/application/models/Detail_model.php
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Function: strpos
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Function: insertAPISummary
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Filename: helpers/my_audit_helper.php
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File: /var/www/html/application/helpers/my_audit_helper.php
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Function: str_replace
File: /var/www/html/application/controllers/Detail.php
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Function: formatAIDetailSummary
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Filename: controllers/Detail.php
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Function: _error_handler
File: /var/www/html/index.php
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Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
Line: 256
Function: _error_handler
File: /var/www/html/index.php
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Filename: controllers/Detail.php
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Function: _error_handler
File: /var/www/html/index.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Message: Undefined array key "usage"
Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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File: /var/www/html/index.php
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Message: Undefined array key "usage"
Filename: controllers/Detail.php
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Function: _error_handler
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Filename: controllers/Detail.php
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File: /var/www/html/index.php
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Filename: controllers/Detail.php
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Line: 260
Function: _error_handler
File: /var/www/html/index.php
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Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
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Function: _error_handler
File: /var/www/html/index.php
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Message: Trying to access array offset on value of type null
Filename: controllers/Detail.php
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Backtrace:
File: /var/www/html/application/controllers/Detail.php
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Function: require_once
Background & Aims: T cells mediate the development of inflammation in inflammatory bowel disease (IBD). We investigated the effects of an antibody against CD3 called otelixizumab, which induces immune tolerance, in intestinal mucosa samples from patients.
Methods: Intestinal tissues were isolated from patients undergoing routine endoscopy or from patients undergoing intestinal surgery for colon cancer or IBD; healthy surrounding tissues were collected as controls. Isolated lamina propria mononuclear cells (LPMCs) and mucosal tissue explants were incubated with otelixizumab for 24 or 48 hours. Production of inflammatory cytokines was determined by enzyme-linked immunosorbent assay. Levels of 36 cytokines and chemokines and phosphorylation of 39 receptor tyrosine kinases and signaling molecules were measured using protein arrays. Immunoblot analysis was used to analyze T-cell transcription factors.
Results: Incubation of intestinal tissues or LPMCs with otelixizumab reduced production of interferon gamma, interleukin (IL)-17A, and other inflammatory cytokines and chemokines, simultaneously increasing production of IL-10. Mucosal biopsy specimens from patients with IBD retained inflammation-associated tyrosine phosphoprotein profiles ex vivo. Incubation of the inflamed tissue with otelixizumab reduced phosphorylation of these proteins to levels observed in control tissues. Otelixizumab also markedly reduced phosphorylation of proteins associated with T-cell receptor activation. Neutralization of IL-10 blocked the anti-inflammatory effects of otelixizumab.
Conclusions: We observed anti-inflammatory effects of anti-CD3 in inflamed intestinal tissues from patients with IBD. The antibody appears to down-regulate T-cell activation via IL-10.
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http://dx.doi.org/10.1053/j.gastro.2014.03.049 | DOI Listing |
Vet Pathol
December 2024
Universidad de León, León, Spain.
The factors that determine the appearance of the different pathologic forms associated with bovine paratuberculosis are not fully understood, but new research suggests a critical role of innate immunity. Toll-like receptors (TLRs) trigger the recognition of invading pathogens by innate immune cells and the onset of specific immune responses. The aim of this work was to assess, immunohistochemically, the expression of TLR1, TLR2, TLR4, and TLR9 in intestinal samples of 20 cows showing different types of paratuberculous lesions: uninfected controls, focal lesions, paucibacillary, and multibacillary diffuse forms.
View Article and Find Full Text PDFFront Immunol
December 2024
Department of Gastrointestinal Surgery, Huadu District People's Hospital, Guangzhou, China.
Gut immunity is essential for maintaining intestinal health. Recent studies have identified that intracellular liquid-liquid phase separation (LLPS) may play a significant role in regulating gut immunity, however, the underlying mechanisms remain unclear. LLPS refers to droplet condensates formed through intracellular molecular interactions, which are crucial for the formation of membraneless organelles and biomolecules.
View Article and Find Full Text PDFFront Vet Sci
December 2024
Department of Animal Sciences, Center for Nutrition and Pregnancy, North Dakota State University, Fargo, ND, United States.
Introduction: Maternal nutrition during pregnancy critically influences offspring development and immune function. One-carbon metabolites (OCM) are epigenetic modifiers that may modulate antimicrobial peptide (AMP) expression, which is vital for innate immunity. This study investigated the effects of maternal nutrient restriction and OCM supplementation on mRNA expression of AMP in fetal and maternal lung, mammary gland, and small intestine of beef cattle.
View Article and Find Full Text PDFJ Transl Med
December 2024
Department of Gastroenterology, The First Affiliated Hospital of Sun Yat-sen University, No. 58 Zhongshan Road 2, Guangzhou, Guangdong, 510080, China.
Background: Previous research on the lower gastrointestinal tract has proved that microbial dysbiosis can lead to intestinal barrier dysfunction and enhanced visceral sensitivity, thus triggering bowel symptoms. Whether esophageal microbial dysbiosis also contributes to the development of gastroesophageal reflux (GER) symptoms, which are known to be associated with impaired esophageal barrier integrity, remains to be explored.
Methods: Patients with GER symptoms (gastroesophageal reflux disease [GERD] and functional esophageal disorders [FED]), duodenal ulcer patients and healthy controls were prospectively included for esophageal microbial analysis.
Biochim Biophys Acta Rev Cancer
December 2024
Gwangju Center, Korea Basic Science Institute, Gwangju 61751, Republic of Korea. Electronic address:
The gut microbiome, a complex community of trillions of microorganisms in the intestines, is crucial in maintaining human health. Recent advancements in microbiome research have unveiled a compelling link between the gut microbiome and cancer development and progression. Alterations in the composition and function of the gut microbiome, known as dysbiosis, have been implicated in various types of cancer, including, esophageal, liver, colon, pancreatic, and gastrointestinal.
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