scholarly journals Blockade of PLD2 Ameliorates Intestinal Mucosal Inflammation of Inflammatory Bowel Disease

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Guangxi Zhou ◽  
Lin Yu ◽  
Wenjing Yang ◽  
Wei Wu ◽  
Leilei Fang ◽  
...  
Keyword(s):  
Peripheral Blood ◽  
Blood Cells ◽  
Inflammatory Diseases ◽  
Critical Role ◽  
Neutrophil Migration ◽  
Mucosal Inflammation ◽  
Peripheral Blood Cells ◽  
Before And After ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Background. Inflammatory bowel diseases (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), are chronically remittent and progressive inflammatory disorders. Phospholipase D2 (PLD2) is reported to be involved in the pathogenesis of several inflammatory diseases. However, the exact role of PLD2 in IBD is obscure.Methods. PLD2 expression was determined in peripheral blood cells and inflamed mucosa from patients with IBD by qRT-PCR. Colonic biopsies were also obtained from CD patients before and after infliximab (IFX) treatment to examine PLD2 expression. PLD2 selective inhibitor (CAY10594) was administrated daily by oral gavage in DSS-induced colitis mice. Bone marrow neutrophils from colitis mice were harvested to examine the migration using Transwell plate.Results. PLD2 was found to be significantly increased in peripheral blood cells and inflamed mucosa in patients with active IBD. Treatment with IFX could significantly decrease PLD2 expression in intestinal mucosa in patients with CD. Moreover, blockade of PLD2 with CAY10594 could markedly ameliorate DSS-induced colitis in mice and promote neutrophil migration.Conclusions. PLD2 plays a critical role in the pathogenesis of IBD. Blockade of PLD2 may serve as a new therapeutic approach for treatment of IBD.

Detection of Apoptosis in Peripheral Blood Cells of 31 Subjects Affected by Down Syndrome Before and After Zinc Therapy

1997 ◽  
Vol 21 (5) ◽  
pp. 449-452 ◽  
Author(s):  
Adriano Antonucci ◽  
Angela Di Baldassarre ◽  
Franco Di Giacomo ◽  
Liborio Stuppia ◽  
Giandomenico Palka
Keyword(s):  
Down Syndrome ◽  
Peripheral Blood ◽  
Blood Cells ◽  
Peripheral Blood Cells ◽  
Before And After

scholarly journals Changes in ABCB1 mRNA Expression in Peripheral Blood Cells before and after Renal Transplantation

2016 ◽  
Vol 39 (7) ◽  
pp. 1085-1090 ◽  
Author(s):  
Hideyuki Kushihara ◽  
Takafumi Kuzuya ◽  
Yuko Miwa ◽  
Kenta Iwasaki ◽  
Yoshihiko Watarai ◽  
...  
Keyword(s):  
Renal Transplantation ◽  
Mrna Expression ◽  
Peripheral Blood ◽  
Blood Cells ◽  
Peripheral Blood Cells ◽  
Before And After

scholarly journals Calprotectin: from biomarker to biological function

Gut ◽  
2021 ◽  
pp. gutjnl-2021-324855
Author(s):  
Almina Jukic ◽  
Latifa Bakiri ◽  
Erwin F. Wagner ◽  
Herbert Tilg ◽  
Timon E. Adolph
Keyword(s):  
Dietary Habits ◽  
Biological Function ◽  
Inflammatory Diseases ◽  
Mucosal Inflammation ◽  
Non Invasive ◽  
Mucosal Surfaces ◽  
Organ Systems ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Substantial Morbidity

The incidence of inflammatory bowel diseases (IBD) emerged with Westernisation of dietary habits worldwide. Crohn’s disease and ulcerative colitis are chronic debilitating conditions that afflict individuals with substantial morbidity and challenge healthcare systems across the globe. Since identification and characterisation of calprotectin (CP) in the 1980s, faecal CP emerged as significantly validated, non-invasive biomarker that allows evaluation of gut inflammation. Faecal CP discriminates between inflammatory and non-inflammatory diseases of the gut and portraits the disease course of human IBD. Recent studies revealed insights into biological functions of the CP subunits S100A8 and S100A9 during orchestration of an inflammatory response at mucosal surfaces across organ systems. In this review, we summarise longitudinal evidence for the evolution of CP from biomarker to rheostat of mucosal inflammation and suggest an algorithm for the interpretation of faecal CP in daily clinical practice. We propose that mechanistic insights into the biological function of CP in the gut and beyond may facilitate interpretation of current assays and guide patient-tailored medical therapy in IBD, a concept warranting controlled clinical trials.

scholarly journals Dichotomous roles of neutrophils in modulating pathogenic and repair processes of inflammatory bowel diseases

2021 ◽  
Author(s):  
Huimin Chen ◽  
Xiaohan Wu ◽  
Chunjin Xu ◽  
Jian Lin ◽  
Zhanju Liu
Keyword(s):  
Immune Cells ◽  
Inflammatory Bowel Diseases ◽  
Intestinal Inflammation ◽  
Critical Role ◽  
Mucosal Inflammation ◽  
Repair Processes ◽  
Microbial Invasion ◽  
Increased Risk ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Abstract Neutrophils are considered as complex innate immune cells and play a critical role in maintaining intestinal mucosal homeostasis. They exert robust pro-inflammatory effects and recruit other immune cells in the acute phase of pathogen infection and intestinal inflammation, but paradoxically, they also limit exogenous microbial invasion and facilitate mucosal restoration. Hyperactivation or dysfunction of neutrophils results in abnormal immune responses, leading to multiple autoimmune and inflammatory diseases including systemic lupus erythematosus, rheumatoid arthritis, and inflammatory bowel diseases (IBD). As a refractory intestinal inflammatory disease, the pathogenesis and progression of IBD are associated with complicated immune response processes in which neutrophils are profoundly involved. However, the consensus on potential roles of neutrophils in modulating pathogenic and repair processes of IBD remains not fully understood. Accumulated infiltrating neutrophils cross the epithelial barrier and contribute to microbial dysbiosis, aggravated intestinal architectural damage, compromised resolution of intestinal inflammation and increased risk of thrombosis during IBD. Paradoxically, activated neutrophils are also associated with effective elimination of invaded microbiota, promoted angiogenesis and tissue restoration of gut mucosa in IBD. Here, we discuss the beneficial and detrimental roles of neutrophils in the onset and resolution of intestinal mucosal inflammation and provide a precise overview of neutrophil functions in the pathogenesis of IBD.

scholarly journals Absence of GdX/UBL4A protects against inflammatory bowel diseases by regulating NF-κB signaling in DCs and macrophages

2018 ◽  
Author(s):  
Chunxiao Liu ◽  
Yifan Zhou ◽  
Mengdi Li ◽  
Ying Wang ◽  
Shigao Yang ◽  
...  
Keyword(s):  
Immune Response ◽  
Inflammatory Diseases ◽  
Adaptor Protein ◽  
Endotoxin Shock ◽  
Innate Immune ◽  
Mucosal Inflammation ◽  
Innate Immune Responses ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Deficient Mice

AbstractNuclear factor-kappa B (NF-κB) activation is critical for innate immune responses. Here we report that the UBL4A (Ubiquitin-like protein 4A, also named GdX) enhances dendritic cells (DCs) and macrophages (Mφ)-mediated innate immune defenses by positively regulating NF-κB signaling. GdX-deficient mice were resistant to LPS-induced endotoxin shock and DSS-induced colitis. DC- or Mφ-specific GdX-deficient mice displayed alleviated mucosal inflammation, and the production of pro-inflammatory cytokines by GdX-deficient DCs and Mφ was reduced. Mechanistically, we found that PTPN2 (TC45) and PP2A form a complex with RelA (p65) to mediate its dephosphorylation whereas GdX interrupts the TC45/PP2A/p65 complex formation and restrict p65 dephosphorylation by trapping TC45. Our study provides a mechanism by which NF-κB signaling is positively regulated by an adaptor protein GdX in DC or Mφ to maintain the innate immune response. Targeting GdX could be a strategy to reduce over-activated immune response in inflammatory diseases.

scholarly journals Colitis following fecal diversion: still a challenge

2000 ◽  
Vol 15 (4) ◽  
pp. 195-200 ◽  
Author(s):  
Leonaldson dos Santos Castro ◽  
Alberto Schanaider ◽  
Bettina Wolff Castro
Keyword(s):  
Inflammatory Diseases ◽  
Fecal Diversion ◽  
Public Hospitals ◽  
Stoma Closure ◽  
Diversion Colitis ◽  
Before And After ◽  
Bowel Diseases ◽  
Intestinal Continuity ◽  
Inflammatory Bowel ◽  
Restoration Of Intestinal Continuity

After fecal diversion, nonspecific colitis may be seen in the defunctionalized colon. The purpose of this prospective study is to identify specific findings that could help in the differential diagnosis between diversion colitis and other inflammatory bowel diseases in order to avoid inappropriate diagnosis and therapy. It was studied, prospectively, thirteen consecutive patients from two public hospitals of Rio de Janeiro who had undergone temporary colostomy for indications other than inflammatory bowel disease. They were submitted to endoscopy with biopsy of both proximal and distal colorectal segments, and prospectively evaluated before and after restoration of intestinal continuity. Endoscopy with biopsy of both proximal and distal excluded colorectal segments showed a nonspecific mucosal and submucosal inflammation, resembling ulcerative colitis ( p < 0.01). There was endoscopic resolution in all patients once restoration of intestinal continuity was established (p < 0.01) and also histologic improvement after the stoma closure. In conclusion there are no specific findings that make possible an unequivocal distinction between diversion colitis and other nonspecific inflammatory diseases. Diagnosis should be achieved if after stoma closure occur remission of endoscopic large bowel inflammatory signs with improvement in mucosal histologic appearance and prompt relief of clinical complaints.

Receptor Mediated Binding of the Fibrinolytic Components, Plasminogen and Urokinase, to Peripheral Blood Cells

1987 ◽  
Vol 58 (03) ◽  
pp. 936-942 ◽  
Author(s):  
Lindsey A Miles ◽  
Edward F Plow
Keyword(s):  
T Cells ◽  
B Cell ◽  
Peripheral Blood ◽  
Binding Sites ◽  
Blood Cells ◽  
High Capacity ◽  
Red Cells ◽  
Peripheral Blood Cells ◽  
Cellular Functions ◽  
Fibrinolytic Proteins

SummaryGlu-plasminogen binds to platelets; the monocytoid line, U937, and the human fetal fibroblast line, GM1380 bind both plasminogen and its activator, urokinase. This study assesses the interaction of these fibrinolytic proteins with circulating human blood cells. Plasminogen bound minimally to red cells but bound saturably and reversibly to monocytes, granulocytes and lymphocytes with apparent Kd values of 0.9-1.4 μM. The interactions were of high capacity with 1.6 to 49 × 105 sites/cell and involved the lysine binding sites of plasminogen. Both T cells and non-rosetting lymphocytes and two B cell lines saturably bound plasminogen. Urokinase bound saturably to gianulocytes, monocytes, non-rosetting lymphocytes and a B cell line, but minimally to T cells, platelets and red cells. Therefore, plasminogen binding sites of high capacity, of similar affinities, and with common recognition specificities are expressed by many peripheral blood cells. Urokinase receptors are also widely distributed, but less so than plasminogen binding sites. The binding ol plasminogen and/ or urokinase to these cells may lead to generation of cell- associated proteolytic activity which contributes to a variety of cellular functions.

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