Review of pulmonary adverse effects of infliximab therapy in Crohn’s disease

Patel, Dhiren; Madani, Shailender; Patel, Shraddha; Guglani, Lokesh

doi:10.1517/14740338.2016.1160053

Cited by 14 publications

(14 citation statements)

References 46 publications

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“…The inhibition of RANKL signaling would be more specific than the inhibition of IL-1β or TNF-α signaling on inflammatory reactions. Therefore, the authors speculate the possibility that RANKL inhibitors may have the advantage of reducing multiple adverse effects that have been identified by the clinical use of nonspecific immunosuppressive agents, such as TNF-α inhibitors [37, 38]. In addition, the anti-RANKL antibody, ‘denosumab’, has been clinically used for osteoporosis patients, and its safety [29–31] and cost-effectiveness compared to other osteoporosis treatments [39, 40] has been reported.…”

Section: Discussionmentioning

confidence: 99%

Expression of the RANK/RANKL/OPG system in the human intervertebral disc: implication for the pathogenesis of intervertebral disc degeneration

Sano

Akeda

Yamada

et al. 2019

BMC Musculoskelet Disord

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Background The expression of the receptor activator of nuclear factor kappa B (RANK) /RANK ligand (RANKL) /osteoprotegerin (OPG) system and its association with the progression of intervertebral disc (IVD) degeneration has recently been reported in a human IVD. However, the effect of the RANK/RANKL/OPG system on the matrix metabolism of human IVD cells, especially on the expression of catabolic factors relevant to IVD degeneration, remains unknown. The purpose of this study was to examine the expression of the RANK/RANKL/OPG system, and then to evaluate the effect of this system on the expression of catabolic factors by human IVD cells. Methods Annulus fibrosus (AF) and nucleus pulposus (NP) cells isolated by sequential enzyme digestion from human IVD tissues obtained during spine surgeries were monolayer cultured. The expression of the RANK/RANKL/OPG system was determined using immunohistochemical methods and real-time polymerase chain reaction (PCR). To evaluate the influence of interleukin-1 beta (IL-1β) stimulation on the mRNA expression of RANK, RANKL, and OPG, recombinant human IL-1β (rhIL-1β) was administered in the culture media of IVD cells. To examine the influence of RANKL signaling on the expression of matrix metalloprotease-3 (MMP-3), MMP-13, and IL-1β, the cells were cultured with exogenous recombinant human RANKL (rhRANKL), recombinant human OPG (rhOPG) or anti-human RANKL mouse monoclonal antibody (ahRANKL-mAB) with or without rhIL-1β. Results Immunoreactivity to RANK/RANKL/OPG and the mRNA expression of the three genes were obviously identified in both AF and NP cells. rhIL-1β stimulation significantly upregulated the mRNA expression level of RANK/RANKL/OPG. The mRNA expression of catabolic factors was significantly upregulated by stimulation of rhRANKL in the presence of rhIL-1β. On the other hand, the administration of either rhOPG or ahRANKL-mAB significantly suppressed the mRNA expression of catabolic factors that had been upregulated by rhIL-1β stimulation. The suppressive effect of ahRANKL-mAB against rhIL-1β stimulation was also confirmed by the protein expression of MMP-3. Conclusions The present study showed that the RANK/RANKL/OPG system may be involved in the progression of IVD degeneration. This study also suggested the potential use of anti-RANKL monoclonal antibody and OPG as therapeutic agents to suppress the progression of IVD degeneration.

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Section: Discussionmentioning

confidence: 99%

Expression of the RANK/RANKL/OPG system in the human intervertebral disc: implication for the pathogenesis of intervertebral disc degeneration

Sano

Akeda

Yamada

et al. 2019

BMC Musculoskelet Disord

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“…Furthermore, results from recent clinical trials confirm that azathioprine is ineffective in UC (Ardizzone et al 2006 ; Kamath et al 2016 ; O’Connor et al 2010 ) and sulfasalazine causes ruptures in liver tissue and decreases platelets count in blood (de Abajo et al 2004 ; Rubin 1994 ). Furthermore, pulmonary disorders are reported in IBD patients treated with chimeric monoclonal antibodies, such as infliximab (Patel et al 2016 ).…”

Section: Introductionmentioning

confidence: 99%

Caffeic acid phenethyl ester is protective in experimental ulcerative colitis via reduction in levels of pro-inflammatory mediators and enhancement of epithelial barrier function

et al. 2017

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BackgroundInhibition of the nuclear factor kappa beta (NF-κβ) pathway has been proposed as a therapeutic target due to its key role in the expression of pro-inflammatory genes, including pro-inflammatory cytokines, chemokines, and adhesion molecules. Caffeic acid phenethyl ester (CAPE) is a naturally occurring anti-inflammatory agent, found in propolis, and has been reported as a specific inhibitor of NF-κβ. However, the impact of CAPE on levels of myeloperoxidases (MPO) and pro-inflammatory cytokines during inflammation is not clear. The aims of this study were to investigate the protective efficacy of CAPE in the mouse model of colitis and determine its effect on MPO activity, pro-inflammatory cytokines levels, and intestinal permeability.MethodDextran sulphate sodium was administered in drinking water to induce colitis in C57/BL6 mice before treatment with intraperitoneal administration of CAPE (30 mg kg−1 day−1). Disease activity index (DAI) score, colon length and tissue histology levels of MPO, pro-inflammatory cytokines, and intestinal permeability were observed.ResultsCAPE-treated mice had lower DAI and tissue inflammation scores, with improved epithelial barrier protection and significant reduction in the level of MPO and pro-inflammatory cytokines.ConclusionOur results show that CAPE is effective in suppressing inflammation-triggered MPO activity and pro-inflammatory cytokines production while enhancing epithelial barrier function in experimental colitis. Thus, we conclude that CAPE could be a potential therapeutic agent for further clinical investigations for treatment of inflammatory bowel diseases in humans.Electronic supplementary materialThe online version of this article (doi:10.1007/s10787-017-0364-x) contains supplementary material, which is available to authorized users.

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“…TNF-α antagonists had several adverse reactions such as serious bacterial infections, tuberculosis, optic neuritis, aplastic anemia, congestive heart failure and multiple cutaneous adverse effects such as eczema, erythema urticaria, lupus-like syndrome, SJS, and TEN [3,[7][8][9]. Especially in pediatric group, several neuropsychiatric disorders, thrombocytopenia, and recurrent viral infection were reported [10].…”

Section: Discussionmentioning

confidence: 99%

Toxic Epidermal Necrolysis complicating Infliximab therapy in Refractory Kawasaki disease

2020

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Severe skin reactions complicating tumor necrosis factor-alpha (TNF-α) antagonist therapy were somewhat reported in adults. We report a case of 24-month-old boy with refractory Kawasaki disease who developed toxic epidermal necrolysis (TEN) after one dose of 5mg/kg infliximab. The patient responded to intravenous hydrocortisone and was able to discharge without any other serious complications. The clinicians should be aware of the potential for severe skin reactions from the use of TNF-α antagonists in children.

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Review of pulmonary adverse effects of infliximab therapy in Crohn’s disease

Cited by 14 publications

References 46 publications

Expression of the RANK/RANKL/OPG system in the human intervertebral disc: implication for the pathogenesis of intervertebral disc degeneration

Expression of the RANK/RANKL/OPG system in the human intervertebral disc: implication for the pathogenesis of intervertebral disc degeneration

Caffeic acid phenethyl ester is protective in experimental ulcerative colitis via reduction in levels of pro-inflammatory mediators and enhancement of epithelial barrier function

Toxic Epidermal Necrolysis complicating Infliximab therapy in Refractory Kawasaki disease

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