La colite ulcérative : une conséquence exceptionnelle après traitement par rituximab

Sekkach, Y.; Hammi, S.; Elqatni, M.; Fatihi, J.; Badaoui, Mohamed; Elomri, N.; Mekouar, F.; Smaali, J.; Jira, M.; Amézyane, T.; Abouzahir, A.; Ghafir, D.

doi:10.1016/j.pharma.2011.06.005

Cited by 13 publications

(6 citation statements)

References 11 publications

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“… 66 , 67 Clinically, the depletion of B cells with anti-CD20 for a variety of disorders has been reported to either exacerbate or lead to the spontaneous onset of colitis. 68 , 69 , 70 , 71 , 72 , 73 , 74 To model this clinical finding, we previously demonstrated that the depletion of B cells in IL-10 −/− mice accelerated the onset of spontaneous colitis. 31 These cumulative studies support our findings that B cells and Tregs are both indispensible in maintaining gut homeostasis.…”

Section: Discussionmentioning

confidence: 98%

T regulatory cells and B cells cooperate to form a regulatory loop that maintains gut homeostasis and suppresses dextran sulfate sodium-induced colitis

et al. 2015

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Regulatory T cells (Tregs) and B cells present in gut-associated lymphoid tissues (GALT) are both implicated in the resolution of colitis. However, how the functions of these cells are coordinated remains elusive. We used the dextran sulfate sodium (DSS)-induced colitis model combined with gene-modified mice to monitor the progression of colitis, and simultaneously examine the number of Tregs and B cells, and the production of IgA antibodies. We found that DSS-treated mice exhibited more severe colitis in the absence of B cells, and that the adoptive transfer of B cells attenuated the disease. Moreover, the transfer of IL-10−/− B cells also attenuated colitis, suggesting that B cells inhibited colitis through an interleukin-10 (IL-10)-independent pathway. Furthermore, antibody depletion of Tregs resulted in exacerbated colitis. Intriguingly, the number of GALT Tregs in B cell-deficient mice was significantly decreased during colitis and the adoptive transfer of B cells into these mice restored the Treg numbers, indicating that B cells contribute to Treg homeostasis. We also found that B cells induced the proliferation of Tregs that in turn promoted B-cell differentiation into IgA-producing plasma cells. These results demonstrate that B cells and Tregs interact and cooperate to prevent excessive immune responses that can lead to colitis.

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Section: Discussionmentioning

confidence: 98%

T regulatory cells and B cells cooperate to form a regulatory loop that maintains gut homeostasis and suppresses dextran sulfate sodium-induced colitis

et al. 2015

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“…The toxicity of many anticancer drugs seriously affects their therapeutic effects and the quality of life in cancer patients ( El Fassi et al, 2008 ; Agathocleous et al, 2010 ; Ardelean et al, 2010 ; Blombery et al, 2011 ; Sekkach et al, 2011 ; Lipka et al, 2016 ; Ziȩtarska et al, 2017 ; Maestá et al, 2018 ; Shahmohammadi et al, 2018 ; Kaegi et al, 2019 ). Some drug treatments lead to intestinal mucosal dysfunction, including endothelial and epithelial cell death and even mucosal immune system activation ( Chaveli-López and Bagán-Sebastián, 2016 ; de Melo Manzi et al, 2016 ; Shimamura et al, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

“…These killing effects are not specific to tumor cells and also affect B cells, T cells, and regulatory T cells. Infection and gastrointestinal toxicity often occur during the course of treatment ( El Fassi et al, 2008 ; Agathocleous et al, 2010 ; Ardelean et al, 2010 ; Blombery et al, 2011 ; Sekkach et al, 2011 ; Lipka et al, 2016 ; Shahmohammadi et al, 2018 ; Kaegi et al, 2019 ), and they can treatment efficacy and patient compliance to a certain extent. However, there is currently no effective treatment to reduce gastrointestinal mucosal lesions.…”

Section: Introductionmentioning

confidence: 99%

Lactobacillus reuteri Alleviates Gastrointestinal Toxicity of Rituximab by Regulating the Proinflammatory T Cells in vivo

et al. 2021

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Rituximab (RTX) is a widely used anticancer drug with gastrointestinal side effects, such as nausea, vomiting, and diarrhea. The reason for these side effects is still poorly understood. Previous studies have reported that the intestinal microbiota is associated with the occurrence of disease and the therapeutic effect of drugs. In this study, we observed mucosal damage, inflammatory cell infiltration and increased intestinal inflammatory factor expression in RTX-treated mice. RTX also changed the diversity of the intestinal microbiota in mice, and decreased abundance of Lactobacillus reuteri was observed in RTX-treated mice. Further experiments revealed that intragastric administration of L. reuteri in RTX-treated mice attenuated the intestinal inflammatory response induced by RTX and regulated the proportion of helper T (Th) cells. In conclusion, our data characterize the effect of the intestinal microbiota on RTX-induced intestinal inflammation, suggesting that modifying the gut microbiota may represent a positive strategy for managing adverse reactions.

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“…Reported adverse effects included fever, chills, mucocutaneous reactions, fatal infusion reactions, and bowel perforation [ 65 , 66 ]. New onset UC and fulminant colitis [ 64 , 67 - 70 ] and an exacerbation of previously documented colitis [ 71 ] have been reported. Also, a severe colitis that developed after rituximab therapy was reported to be related to an infectious torovirus agent [ 66 ].…”

Section: Anti-tumoral Agentsmentioning

confidence: 99%

“…These cases suggest that there is a protective effect of CD20+ lymphocytes in the gut and implicate that their depletion leads to the development and exacerbation of IBD. Clinical and histologic features of rituximab-associated colitis are summarized in Tables 4 and 5 [ 62 - 64 , 66 - 70 ].…”

Section: Anti-tumoral Agentsmentioning

confidence: 99%

Anti-Inflammatory Biologics and Anti-Tumoral Immune Therapies-Associated Colitis: A Focused Review of Literature

et al. 2018

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An increasing number of drugs including monoclonal antibodies and small molecules, either anti-inflammatory or immunity-enhancing, have been developed to treat human diseases and the number of medications in these classes is likely to expand in the future. The two most commonly used categories of such therapies are the anti-inflammatory group (anti- tumor necrosis factor (TNF) α, anti-interleukins/interleukin receptors, and anti-integrin bodies) and the anti-tumoral agents (immune checkpoint inhibitors, anti-CD20, and anti-endothelial growth factor). Although the anti-inflammatory biologics have brought about a revolutionary effect in the management of a variety of autoimmune disorders including rheumatologic diseases, inflammatory bowel disease, and inflammatory dermatological diseases, their ability to induce colitis in patients without a prior history of colitis or exacerbate quiescent colitis has been increasingly and unexpectedly recognized. While the use of immune-augmenting monoclonal antibody therapies results in a significant survival benefit in a subset of patients with malignancies, these monoclonal antibodies also have the ability to cause colitis through an apparent autoimmune mechanism. Colitis associated with these medications may demonstrate multiple histologic patterns including increased apoptosis (graft versus host disease (GVHD)-like), autoimmune enteropathy pattern, acute colitis pattern, ischemic colitis, inflammatory bowel disease pattern, either ulcerative colitis-like, Crohn’s disease-like, or fulminant colitis-like. In addition, anti-inflammatory biologics are known to cause or reactivate latent infections such as tuberculosis and increase the risk for malignancies including high-grade lymphomas as well as indolent lymphoproliferative disorders. Thus, the differential diagnosis for colitis in patients receiving therapeutic anti-inflammatory biologics or anti-tumoral agents can be broad. Optimal diagnosis and treatment requires a multidisciplinary approach. This review aims to provide an overview of the literature on the clinical features, histology, and treatment of these newly recognized anti-inflammatory biologic and anti-tumoral immune therapy-induced colitises and hopes this outlines will raise the vigilance of all clinicians of these entities.

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La colite ulcérative : une conséquence exceptionnelle après traitement par rituximab

Cited by 13 publications

References 11 publications

T regulatory cells and B cells cooperate to form a regulatory loop that maintains gut homeostasis and suppresses dextran sulfate sodium-induced colitis

T regulatory cells and B cells cooperate to form a regulatory loop that maintains gut homeostasis and suppresses dextran sulfate sodium-induced colitis

Lactobacillus reuteri Alleviates Gastrointestinal Toxicity of Rituximab by Regulating the Proinflammatory T Cells in vivo

Anti-Inflammatory Biologics and Anti-Tumoral Immune Therapies-Associated Colitis: A Focused Review of Literature

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