Factor H inhibits complement activation induced by liposomal and micellar drugs and the therapeutic antibody rituximab in vitro

Mészáros, Tamás; Csincsi, Ádám I.; Uzonyi, Barbara; Hebecker, Mario; Fülöp, Tamás; Erdei, Anna; Szebeni, János; Józsi, Mihály

doi:10.1016/j.nano.2015.11.019

Cited by 23 publications

(25 citation statements)

References 42 publications

(47 reference statements)

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“…Then, the anaphylatoxins bind to secretory cells (mast cells, basophils, macrophages, other phagocytic cells, and leukocytes) leading to the release/production of a multitude of secondary mediators (including histamine, tryptase, platelet-activating factor, thromboxane A 2 , leukotrienes (LTs), cytokines, proteases, and prostaglandins) [14,15]. The complement cascade can be triggered by the classical pathway (CP), lectin pathway (LP) or alternative pathway (AP) [16] in which complement component 3 (C3) plays an important role (Fig. 1).…”

Section: Mechanisms Of Pseudoallergymentioning

confidence: 99%

“…CARPA can be a severe syndrome involving several cardio pulmonary symptoms that include pulmonary edema, hypotension, arrhythmia, airway occlusion, respiratory distress, and potential cardiac arrest, which may eventually lead to anaphylactic cardiogenic shock and death in severe cases [16]. Intravenous injection of nanotechnology drugs (liposomal, micellar) may induce CARPA [14].…”

Section: Drug-induced Pseudoallergymentioning

confidence: 99%

“…The most well-known liposomal drugs are ambisome and doxil, and the micelle-solubilized-drug taxol [14]. Ambisome, a charged non-PEGylated liposome, induces CARPA via AP [16,59]. Factor H inhibits complement activation induced by the antifungal drugs ambisome and taxol [16].…”

Section: Drug-induced Pseudoallergymentioning

confidence: 99%

“…Ambisome, a charged non-PEGylated liposome, induces CARPA via AP [16,59]. Factor H inhibits complement activation induced by the antifungal drugs ambisome and taxol [16]. Doxil, one of the PEG-PL-engineered nanomedicines, triggers the complement activation in human serum through both CP and AP [21].…”

Section: Drug-induced Pseudoallergymentioning

confidence: 99%

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Drug-Induced Pseudoallergy: A Review of the Causes and Mechanisms

Zhang

Li²,

Shi³

et al. 2017

Pharmacology

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Adverse drug reactions occur frequently and can trigger pseudoallergy, which has become a serious threat to public health. Pseudoallergy is a typical non-immune anaphylactic reaction characterized by the independence of antigen-specific immune responses. In the clinic, pseudoallergy is often elicited by the first dose of medication, and here lies its unpredictability and occasional lethal outcome. However, the mechanisms of pseudoallergy are not well understood. This review focusses on the causes and mechanisms of pseudoallergy induced by drugs. Two categories of mechanisms will be considered, namely, (1) complement activation-related pseudoallergy and (2) mast cell activation-related pseudoallergy. The factors that induce pseudoallergy include opioid drugs, complement activation-related pseudoallergenic drugs, nonsteroidal anti-inflammatory drugs and traditional Chinese medicine injections.

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Section: Mechanisms Of Pseudoallergymentioning

confidence: 99%

Section: Drug-induced Pseudoallergymentioning

confidence: 99%

Section: Drug-induced Pseudoallergymentioning

confidence: 99%

Section: Drug-induced Pseudoallergymentioning

confidence: 99%

See 2 more Smart Citations

Drug-Induced Pseudoallergy: A Review of the Causes and Mechanisms

Zhang

Li²,

Shi³

et al. 2017

Pharmacology

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“…Importantly, one group showed no impact of CFHR1 on rituximab-induced complement activation(35). This supports our finding that CFHR1 does not associate with differential outcome in patients treated with obinutuzumab, but may associate with rituximab outcome as observed in the observational cohort.…”

Section: Discussionmentioning

confidence: 99%

Complement-Regulatory Proteins CFHR1 and CFHR3 and Patient Response to Anti-CD20 Monoclonal Antibody Therapy

Rogers

Mott

Smith

et al. 2017

Clinical Cancer Research

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Purpose Anti-CD20 monoclonal antibody (mAb) therapies, including rituximab and obinutuzumab (GA101) are common treatments for follicular lymphoma (FL). In an effort to better understand the role of complement in mAb action, we recently performed germline SNP profiling on 142 FL patients and found rs3766404 genotype correlated with patient response to rituximab. To assess the role of three SNP-associated complement regulatory proteins (CFH, CFHR1 and CFHR3) in clinical response to anti-CD20 mAb, we studied two cohorts of patients treated with anti-CD20 mAb. Experimental Design Cohorts included the Iowa/Mayo Lymphoma SPORE observational cohort of subjects with a new diagnosis of FL treated with rituximab, and the GAUSS prospective randomized trial cohort of FL subjects randomized to receive single agent rituximab or obinutuzumab. Circulating protein expression was measured for CFH, CFHR1 and CFHR3 and correlated to clinical outcome. Results rs3766404 genotype correlated with expression of the related downstream genes CFHR1 and CFHR3. Loss of CFHR1 expression correlated with inferior patient outcome in the observational cohort, but not in the GAUSS cohort. Loss of CFHR3 correlated with superior event-free survival in GAUSS subjects treated with obinutuzumab, but not rituximab. Conclusions We conclude that the relationship between complement regulatory proteins CFHR1 and CFHR3 and response to anti-CD20 mAb therapy varies based on the specific anti-CD20 mAb used. We propose that CFHR3 is a candidate biomarker for obinutuzumab response. Further studies are needed to validate these findings and to better understand how complement pathways and complement regulatory proteins impact on the efficacy of anti-CD20 mAb therapy.

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Exploring and Analyzing the Systemic Delivery Barriers for Nanoparticles

Wang,

Quine,

Frickenstein

et al. 2023

Adv Funct Materials

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Most nanomedicines require efficient in vivo delivery to elicit meaningful diagnostic and therapeutic effects. However, en route to their intended tissues, systemically administered nanoparticles often encounter delivery barriers. To describe these barriers, the term “nanoparticle blood removal pathways” (NBRP) is proposed, which summarizes the interactions between nanoparticles and the body's various cell‐dependent and cell‐independent blood clearance mechanisms. Nanoparticle design and biological modulation strategies are reviewed to mitigate nanoparticle‐NBRP interactions. As these interactions affect nanoparticle delivery, the preclinical literature from 2011–2021 is studied, and the nanoparticle blood circulation and organ biodistribution data are analyzed. The findings reveal that nanoparticle surface chemistry affects the in vivo behavior more than other nanoparticle design parameters. Combinatory biological‐PEG surface modification improves the blood area under the curve by ≈418%, with a decrease in liver accumulation of up to 47%. A greater understanding of nanoparticle‐NBRP interactions and associated delivery trends will provide new nanoparticle design and biological modulation strategies for safer, more effective, and more efficient nanomedicines.

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Factor H inhibits complement activation induced by liposomal and micellar drugs and the therapeutic antibody rituximab in vitro

Cited by 23 publications

References 42 publications

Drug-Induced Pseudoallergy: A Review of the Causes and Mechanisms

Drug-Induced Pseudoallergy: A Review of the Causes and Mechanisms

Complement-Regulatory Proteins CFHR1 and CFHR3 and Patient Response to Anti-CD20 Monoclonal Antibody Therapy

Exploring and Analyzing the Systemic Delivery Barriers for Nanoparticles

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