Mobilization of Bone Marrow Cells by Leukocytapheresis in Patients With Ulcerative Colitis

Mitsuyama, Keiichi; Andoh, Akira; Masuda, Junko; Yamasaki, Hiroshi; Kuwaki, Kotaro; Takedatsu, Hidetoshi; Seki, Ritsuko; Nishida, Hidemi; Takahashi, Osamu; Sata, Michio

doi:10.1111/j.1744-9987.2008.00587.x

Cited by 14 publications

(9 citation statements)

References 37 publications

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“…This is similar to the previous studies in patients with rheumatoid arthritis and ulcerative colitis and healthy volunteers (23)(24)(25). It has been reported that the peripheral blood platelets were removed while passing through the column (26). We considered that thrombocytopenia was recovered by producing new platelets in bone marrow.…”

Section: Discussionsupporting

confidence: 75%

Leukocytapheresis for the treatment of acute exacerbation of idiopathic interstitial pneumonias: a pilot study

et al. 2017

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: Objective : Idiopathic interstitial pneumonias (IIPs) are a group of heterogeneous diffuse parenchymal lung disorders of unknown etiology. An acute exacerbation (AE) is an acute respiratory deterioration that occurs in IIPs. The prognosis of AE of IIPs (AE-IIPs) is extremely severe ; however, no established therapies exist. We aimed to evaluate the efficacy of leukocytapheresis (LCAP) to treat patients with AE-IIPs. Patients and Methods : Six chronic IIPs patients who developed AE were enrolled in this study. We performed LCAP on days 2, 3, 9 and 10 in all six patients. All patients were also treated with high-dose corticosteroids and a continuous administration of low-molecular-weight heparin. We observed 30-day survival after the diagnosis of AE to evaluate the efficacy of LCAP. We also assessed oxygenation, high-resolution computed tomography (HRCT) findings, and certain chemical mediators in the peripheral blood. Results : Five of six patients survived more than 30 days. One patient died of progressive respiratory failure. Oxygenation and HRCT findings tended to improve in all survivors. The serum levels of lactate dehydrogenase, high mobility group box -1, and interleukin -18 were significantly decreased statistically post-LCAP. No severe adverse events occurred. Conclusion : We suggest that LCAP is a safe and effective therapy for treating patients with AE-IIPs.

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Section: Discussionsupporting

confidence: 75%

Leukocytapheresis for the treatment of acute exacerbation of idiopathic interstitial pneumonias: a pilot study

et al. 2017

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“…1b) individual leukocyte fractions were almost 100% for granulocytes and monocytes, and 73-100% for lymphocytes. These data indicate that the column absorbs the leukocytes similar to the removal rate in humans [19]. In addition, the removal capacity of platelets was more potent in the rat column than in the human column.…”

Section: Removal Rate Of Blood Cellssupporting

confidence: 53%

“…hematopoietic stem cells in the bone marrow and bone marrow-derived EPCs in the circulation, providing direct evidence that LCAP stimulates hematopoiesis. LCAP in UC does not change cytokine levels that influence mobilization from bone marrow or from the marginated pool [19]. Interestingly, CGRP directly acts on hematopoietic progenitor cells to promote formation of granulomonocytic colonies [33], and may also stimulate hematopoiesis during LCAP.…”

Section: Discussionmentioning

confidence: 98%

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Mechanisms Underlying the Effects of Leukocyte Apheresis with a Fiber Filter in a Rat Model of Dextran Sulfate Sodium-Induced Colitis

et al. 2009

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While several clinical trials have suggested that leukocytapheresis (LCAP) by filtration can benefit patients with active ulcerative colitis, the mechanisms underlying these benefits are largely unknown. The aim of this study was to address the mechanisms that may underlie the therapeutic effects of LCAP using a dextran sulfate sodium-induced colitis model in rats. Treatment with the active column, but not the sham column, improved disease severity by down-regulating pro-inflammatory events, including the cell-proliferative responses and inflammatory cytokine and reactive oxygen production, as well as by up-regulating protective events, including hepatocyte growth factor production, bone marrow-derived endothelial progenitor cell induction, and colonic blood flow levels, which were mediated predominantly by calcitonin gene-related peptide. The improvement was also associated with the increase of Ki-67 labeling in the colonic epithelium. In conclusion, the LCAP procedure was used in a dextran sulfate sodium-induced colitis model in rats under extracorporeal circulation conditions. This approach down-regulated pro-inflammatory events and up-regulated protective events in association with disease improvement. These data suggest that LCAP is feasible in animals and should shed light on the mechanisms of LCAP in clinical settings.

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“…Together, our data questions the relevance of IL-13 and highlights the role of IL-6 in UC [27,44,45] suggesting that UC may be characterized by a mixed profile rather than a Th2 cytokine profile [46,47]. Although current therapies for UC patients involve systemic administration of anti-TNF-α, anti-IL-6 (alone or in combination with TNF-α) is revealed as potentially more efficient as some authors have recently reported [48][49][50].In summary, our data questions the concept of UC as a Th2 disease and the relevance of IL-13 in its etiology, highlighting the role of IL-6 as a central cytokine controlling the local immune response. Our results confirmed that the tissue microenvironment conditions the phenotype and function of DCs.…”

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confidence: 69%

IL‐6 promotes immune responses in human ulcerative colitis and induces a skin‐homing phenotype in the dendritic cells and Tcells they stimulate

et al. 2012

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Dendritic cells (DCs) control the type and location of immune responses. Ulcerative colitis (UC) is considered a Th2 disease mediated by IL-13 where up to one third of patients can develop extraintestinal manifestations. Colonic biopsies from inflamed and noninflamed areas of UC patients were cultured in vitro and their supernatants were used to condition human blood enriched DCs from healthy controls. Levels of IL-13 in the culture supernatants were below the detection limit in most cases and the cytokine profile suggested a mixed profile rather than a Th2 cytokine profile. IL-6 was the predominant cytokine found in inflamed areas from UC patients and its concentration correlated with the Mayo endoscopic score for severity of disease. DCs conditioned with noninflamed culture supernatants acquired a regulatory phenotype with decreased stimulatory capacity. However, DCs conditioned with inflamed culture supernatants acquired a proinflammatory phenotype with increased expression of the skin-homing chemokine CCR8. These DCs did not have decreased T-cell stimulatory capacity and primed T cells with the skin-homing CLA molecule in an IL-6-dependent mechanism. Our results highlight the role of IL-6 in UC and question the concept of UC as a Th2 disease and the relevance of IL-13 in its etiology.Keywords: Dendritic cells r IL-6 r Mucosal immunity r Intestinal immunity r Ulcerative colitis Correspondence: Prof. Stella C. Knight e-mail: s.knight@imperial.ac.uk IntroductionThe gastrointestinal tract is in contact with a wide variety of commensal microbiota and diverse pathogens, and therefore C 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim www.eji-journal.eu 1338 David Bernardo et al. Eur. J. Immunol. 2012. 42: 1337-1353 requires a balance to be maintained between immunity and immune tolerance; the lack of immune responses against food antigens and/or the commensal microbiota is essential to maintain the homeostasis of the gastrointestinal tract [1]. Ulcerative colitis (UC) is a form of inflammatory bowel disease (IBD), traditionally related to a Th2 cytokine profile mediated by 3], where immune homeostasis of the gastrointestinal tract is compromised. Up to 1/3rd of UC patients can develop extraintestinal manifestations with the skin being one of such tissues [4,5].Dendritic cells (DCs) are the most potent antigen presenting cells and determine the nature and type of immune responses [6,7]. Intestinal DCs control immune tolerance in the gastrointestinal tract [8][9][10]. DCs also maintain immune responses localized to specific tissues, since they imprint specific tissue-homing profiles on stimulated T cells [11]. Retinoic acid (RA), the active form of vitamin A following dehydrogenization by the RALDH2 enzyme controls some of the mechanisms of immune homeostasis of the gut [12][13][14]. RA-producing DCs mediate the IgA switching of B cells [15], the generation of T cells with a regulatory phenotype [10], and the imprinting of gut-homing markers on B and T cells [16,17], thereby keeping tolerogenic immune responses com...

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Mobilization of Bone Marrow Cells by Leukocytapheresis in Patients With Ulcerative Colitis

Cited by 14 publications

References 37 publications

Leukocytapheresis for the treatment of acute exacerbation of idiopathic interstitial pneumonias: a pilot study

Leukocytapheresis for the treatment of acute exacerbation of idiopathic interstitial pneumonias: a pilot study

Mechanisms Underlying the Effects of Leukocyte Apheresis with a Fiber Filter in a Rat Model of Dextran Sulfate Sodium-Induced Colitis

IL‐6 promotes immune responses in human ulcerative colitis and induces a skin‐homing phenotype in the dendritic cells and Tcells they stimulate

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