bioRxiv ScienceSearch

bioRxiv · 10.1101/613190

A novel reporter gene assay for pyrogen detection

Abstract

Fever is a systemic inflammatory response of the body to pyrogens. Nuclear factor {kappa}B (NF-{kappa}B) is a central signalling molecule that causes the excessive secretion of various proinflammatory factors induced by pyrogens. This study explored the feasibility of a novel reporter gene assay (RGA) for pyrogen detection using RAW 264.7 cells stably transfected with the NF-{kappa}B reporter gene as a pyrogenic marker. Pyrogen was incubated with the transgenic cells, and the intensity of the fluorescence signal generated by luciferase secreted by the reporter gene was used to reflect the degree of activation of NF-{kappa}B, so as to quantitatively detect the pyrogens. The RGA could detect different types of pyrogens, including the lipopolysaccharide (LPS) of gram-negative bacteria, the lipoteichoic acid (LTA) of gram-positive bacteria, and the zymosan of fungi, and a good dose-effect relationship was observed in terms of NF-{kappa}B activity. The limits of detection of the RGA to those pyrogens were 0.03 EU/ml, 0.001 g/ml, and 1 g/ml, respectively. The method had good precision and accuracy and could be applied to many biological products (e.g., nivolumab, rituximab, bevacizumab, etanercept, basiliximab, haemophilus influenzae type b conjugate vaccine, 23-valent pneumococcal polysaccharide vaccine, and group A and group C meningococcal conjugate vaccine). The results of this study suggest that the novel RGA has a wide pyrogen detection spectrum and is sufficiently sensitive, stable, and accurate for various applications.\n\nImportancePyrogen testing is mandatory and a critical method to ensure the safety of parenteral products including vaccines.\n\nCurrently, only two pharmacological tests, including the rabbit pyrogen test and the bacterial endotoxins test (BET), are applied to evaluate pyrogenic contamination in parenteral pharmaceuticals by most of state pharmacopoeias. Although generally reliable, both of these assays have shortcomings. The rabbit test is not quantitative but is expensive and involves the use of animals. It can also produce varying responses depending on the strain, age and housing conditions of the rabbits. The BET, however, does not detect pyrogens other than gram-negative bacterial endotoxins and is often problematic when used to test solutions with a high protein content.\n\nTo overcome these shortcomings and satisfy the growing need for new methods prompted by the constantly increasing production of biological compounds, it is necessary to develop the novel assay for pyrogen detection.\n\nHighlightsO_LIThis novel reporter gene assay can detect different types of pyrogens, including the lipopolysaccharide of gram-negative bacteria, the lipoteichoic acid of gram-positive bacteria, and the zymosan of fungi.\nC_LIO_LIThe novel reporter gene assay is sufficiently sensitive, stable, and accurate for various applications.\nC_LI

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

He, Q., Yu, F. C., Wang, L., Ni, B. Y., Zhang, H., Du, Y., Gao, H., Wang, Z. J.. 2019-04-18. A novel reporter gene assay for pyrogen detection. https://doi.org/10.1101/613190

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

De novo design of CR2 binder as vaccine scaffold

Efficient B cell activation during vaccine-induced humoral immunity relies on both B cell receptor (BCR) antigen recognition and synergistic signaling from co-receptors. Complement receptor 2 (CR2), the primary BCR co-receptor on B cells, lowers the activation threshold and amplifies downstream kinase signaling by orders of magnitude when engaged by complement fragment C3d decorated antigens. Targeting CR2 therefore represents a rational vaccine enhancement strategy, yet native C3d suffers from low affinity, poor stability, and manufacturing challenges. Here, we report the de novo design of a highly stable, high-affinity CR2 binder using deep learning driving protein design methods. Biophysical characterization, high-resolution cryoEM structural determination, and functional assays in vitro and in vivo confirm that the designed binder matches computational design models and specifically engages CR2 to boost B cell activation. When fused to antigen as a vaccine scaffold, the trimeric CR2 binder elicits robust humoral immune responses comparable to nanoparticle vaccines, while retaining the simplicity of single-chain protein production. Our work establishes a modular CR2 targeting vaccine scaffold platform with broad translational potential for next-generation protein vaccines.

immunology

Chronic opioid-associated immune dysregulation among people living with HIV

Objectives: Persistent immune dysregulation contributes to chronic disease among people living with HIV (PWH), even after viral suppression with antiretroviral therapy (ART). Although chronic opioid exposure is associated with adverse clinical outcomes, its impact on immune homeostasis during ART remains incompletely understood. We investigated whether opioid use disorder (OUD) is associated with persistent systemic and cellular immune dysregulation despite ART-mediated reductions in HIV viral load (VL). Methods: Peripheral blood was collected longitudinally from PWH with OUD (PWH/OUD+) and detectable HIV VL during 6 months of optimized ART (months 0, 3, and 6). A reference cohort of PWH without OUD (PWH/OUD-) and suppressed HIV VL provided a single blood sample. Immune profiling included plasma inflammatory biomarkers, multiplex cytokine analyses, spectral flow cytometry, and assessment of monocyte cytokine responses following lipopolysaccharide (LPS) stimulation. Mixed-effects models adjusted for HIV VL and VL-stratified analyses were performed. Results: PWH/OUD+ exhibited persistent immune dysregulation despite reductions in HIV VL. Plasma sCD163, sCD14, fractalkine, and I-TAC remained elevated, whereas TGF-{beta}1 was reduced. OUD was associated with expansion of CD16 monocytes and altered expression of CCR2, CD38, and CD11b. CD4 and CD8 T cells, NK cells, and B cells also exhibited persistent alterations in markers of activation, metabolism, and trafficking. Monocytes from PWH/OUD+ displayed attenuated cytokine responses following LPS stimulation. Conclusions: OUD is associated with persistent systemic and cellular immune dysfunction in PWH despite ART-mediated viral suppression, supporting opioid exposure as an independent contributor to chronic immune dysregulation that may promote inflammation, immune dysfunction, and long-term HIV-associated comorbidities. Keywords: HIV, Opioid-use disorder, innate immunity, cytokine

immunology

The mitochondrial RNA extrusion-induced innate immunity is regulated by N6-methyladenosine machinery

Mitochondrial RNA (mtRNA) released into the cytosol functions as a damage associated molecular pattern that activates pattern-recognition receptor (PRR)-mediated inflammation, yet its release mechanisms and cytoplasmic fate remain poorly understood. Here we report that chemical Abt-373-treatment and Vesicular stomatitis virus (VSV) infection induce mtRNA extrusion through Bax/Bak and VDAC1 channels, accompanied by mtDNA release. Extruded mtRNA in A549 cells activates multiple cytosolic PRRs, including RIG-I, MDA5, TLR3/7/8, and PKR, each contributing differentially to the innate immune signaling. Analysis of GEO datasets and methylated RNA immunoprecipitation (MeRIP) assays further reveals that mtRNA carries methyladenosine (m6A) modification. m6A machinery proteins are involved in the cytoplasmic retention time of mtRNA and its interaction with RIG-I, thereby modulating mtRNA-induced innate immunity. Thus, our work establishes in vitro models of mtRNA extrusion, and highlights m6A-dependent modulation as a potential therapeutic target for mtRNA-driven inflammation.

immunology