About

Amanda M. Jamieson, Ph.D., is an Associate Professor in the Department of Molecular Microbiology and Immunology at Brown University. She earned her B.A. in Biology from Carleton College in 1997 and completed her Ph.D. in Molecular and Cell Biology in 2003. As the Principal Investigator of the Jamieson Lab, she leads a research team that includes senior research associates, graduate students, and undergraduate researchers. Her lab focuses on advancing the understanding of molecular microbiology and immunology, contributing to the academic community at Brown University through both research and mentorship.

Research topics

• Internal medicine
• Virology
• Medicine
• Intensive care medicine
• Biology
• Genetics

Selected publications

• Comparative Analysis of Inflammatory Response in Surgical Wound Drainage Fluid in Scoliosis Surgery: A Study of Neuromuscular vs. Idiopathic Patients

  medRxiv · 2025-04-11

  preprintOpen accessSenior authorCorresponding

  Abstract This study examines immune and inflammatory responses in draining wound fluid over the course of the early stages of wound healing in patients recovering from spinal fusion surgery. The inflammatory phase of wound healing is essential for setting the stage for successful tissue repair and preventing chronic or poorly healing wounds. Scoliosis can be idiopathic or occur secondary to neuromuscular disorders, which are known to be associated with poor wound healing outcomes. We hypothesized that neuromuscular scoliosis patients would exhibit differences in inflammatory wound healing markers compared to idiopathic scoliosis patients. Comparison of the cellular and cytokine contents of draining wound fluid revealed that several inflammatory cytokines were elevated in the neuromuscular scoliosis patient group compared to idiopathic, whereas the leukocyte contents were the same between groups. This study shows that draining wound fluid is a good source of cellular and soluble biomarkers for acute wound healing and can be used to determine changes in individuals at risk for wound healing complications.

  PublisherOA PDFDOI

• The impact of pH on proteolytic activity in wound fluid: Implications for acid therapy

  Journal of Biological Chemistry · 2025-09-16 · 1 citations

  articleOpen access

  Wound healing necessitates a balance between synthesis and breakdown of extracellular matrix components, which is tightly regulated by proteases and their inhibitors. While studies have demonstrated that citric and acetic acid treatments enhance healing in recalcitrant wounds, the underlying proteolytic mechanisms remain elusive. In this study, we systematically evaluated changes in the proteolytic activity of murine wound fluid upon acidification. A library of 228 synthetic peptides served as reporters of protease activity at pH 7.4, pH 5.0, and pH 3.5. The peptide digestion patterns differed at each pH, revealing that proteases active at pH 7.4 are inactivated at pH 3.5. Notably, cathepsin D emerged as the dominant active enzyme at pH 3.5, and its activity was inhibited by pepstatin. Using a fluorogenic substrate, we quantified cathepsin D activity across varying pH levels and demonstrated optimal activity between pH 3.0 and 3.8. This activity was detectable as early as 1 day postinjury and persisted over the following 10 days. Importantly, human wound fluid exhibited the same activity profile, validating the mouse model as a relevant system for studying acid-mediated wound healing processes.

  PublisherOA PDFDOI

• Comparative Analysis of Inflammatory Response in Surgical Wound Drainage Fluid in Scoliosis Surgery: A Study of Neuromuscular vs. Idiopathic Patients

  Wound Repair and Regeneration · 2025-07-01

  articleOpen accessSenior authorCorresponding

  This study examines immune and inflammatory responses in draining wound fluid over the course of the early stages of wound healing in patients recovering from spinal fusion surgery. The inflammatory phase of wound healing is essential for setting the stage for successful tissue repair and preventing chronic or poorly healing wounds. Scoliosis can be idiopathic or occur secondary to neuromuscular disorders, which are known to be associated with poor wound healing outcomes. We hypothesised that neuromuscular scoliosis patients would exhibit differences in inflammatory wound healing markers compared to idiopathic scoliosis patients. Comparison of the cellular and cytokine contents of draining wound fluid revealed that several inflammatory cytokines were elevated in the neuromuscular scoliosis patient group compared to idiopathic, whereas the leukocyte contents were the same between groups. This study shows that draining wound fluid is a good source of cellular and soluble biomarkers for acute wound healing and can be used to determine changes in individuals at risk for wound healing complications.

  PublisherOA PDFDOI

• Norovirus co-opts NINJ1 for selective protein secretion

  Science Advances · 2025-02-28 · 6 citations

  articleOpen access

  Plasma membrane rupture by Ninjurin-1 (NINJ1) executes programmed cell death, releasing large cellular damage-associated molecular patterns (DAMPs). However, the regulation and selectivity of NINJ1-mediated DAMP release remain unexplored. Here, we uncover that murine norovirus (MNoV) strategically co-opts NINJ1 to selectively release the intracellular viral protein NS1, while NINJ1-mediated plasma membrane rupture simultaneously bulk-releases various cellular DAMPs. Host caspase-3 cleaves the precursor NS1/2, leading to NS1 secretion via an unconventional pathway. An unbiased CRISPR screen identifies NINJ1 as an essential factor for NS1 secretion. During infection, NINJ1 is recruited to the viral replication site, where it oligomerizes and forms speckled bodies, directly interacting with NS1. Subsequent mutagenesis studies identify critical amino acid residues of NS1 necessary for its interaction with NINJ1 and selective secretion. Genetic ablation or pharmaceutical inhibition of caspase-3 inhibits oral MNoV infection in mice. This study underscores the co-option of NINJ1 for controlled release of an intracellular viral protein.

  PublisherOA PDFDOI

• Machine Learning Assisted Spectral Fingerprinting for Immune Cell Phenotyping

  bioRxiv (Cold Spring Harbor Laboratory) · 2024-03-08

  preprintOpen access

  Abstract Spectral fingerprinting has emerged as a powerful tool, adept at identifying chemical compounds and deciphering complex interactions within cells and engineered nanomaterials. Using near-infrared (NIR) fluorescence spectral fingerprinting coupled with machine learning techniques, we uncover complex interactions between DNA-functionalized single-walled carbon nanotubes (DNA-SWCNTs) and live macrophage cells, enabling in situ phenotype discrimination. Through the use of Raman microscopy, we showcase statistically higher DNA-SWCNT uptake and a significantly lower defect ratio in M1 macrophages as compared to M2 and naïve phenotypes. NIR fluorescence data also indicate that distinctive intra-endosomal environments of these cell types give rise to significant differences in many optical features such as emission peak intensities, center wavelengths, and peak intensity ratios. Such features serve as distinctive markers for identifying different macrophage phenotypes. We further use a support vector machine (SVM) model trained on SWCNT fluorescence data to identify M1 and M2 macrophages, achieving an impressive accuracy of > 95%. Finally, we observe that the stability of DNA-SWCNT complexes, influenced by DNA sequence length, is a crucial consideration for applications such as cell phenotyping or mapping intra-endosomal microenvironments using AI techniques. Our findings suggest that shorter DNA-sequences like GT 6 give rise to more improved model accuracy (> 87%) due to increased active interactions of SWCNTs with biomolecules in the endosomal microenvironment. Implications of this research extend to the development of nanomaterial-based platforms for cellular identification, holding promise for potential applications in real time monitoring of in vivo cellular differentiation. TOC Graphic

  PublisherOA PDFDOI

• Peripheral Ca _V 2.2 Channels in the Skin Regulate Prolonged Heat Hypersensitivity during Neuroinflammation

  eNeuro · 2024-10-21 · 4 citations

  articleOpen access

  Neuroinflammation can lead to chronic maladaptive pain affecting millions of people worldwide. Neurotransmitters, cytokines, and ion channels are implicated in neuroimmune cell signaling, but their roles in specific behavioral responses are not fully elucidated. Voltage-gated Ca V 2.2 channel activity in skin controls rapid and transient heat hypersensitivity induced by intradermal (i.d.) capsaicin via IL-1ɑ cytokine signaling. Ca V 2.2 channels are not, however, involved in mechanical hypersensitivity that developed in the i.d. capsaicin animal model. Here, we show that Ca V 2.2 channels are also critical for heat hypersensitivity induced by i.d. complete Freund adjuvant (CFA). i.d. CFA, a model of chronic neuroinflammation, involves ongoing cytokine signaling for days leading to pronounced edema and hypersensitivity to sensory stimuli. Peripheral Ca V 2.2 channel activity in the skin was required for the full development and week-long time course of heat hypersensitivity induced by i.d. CFA, but paw edema and mechanical hypersensitivity were independent of Ca V 2.2 channel activity. CFA induced increases in several cytokines in hindpaw fluid including IL-6 which was also dependent on Ca V 2.2 channel activity. Using IL-6–specific neutralizing antibodies in vivo, we show that IL-6 contributes to heat hypersensitivity and that neutralizing both IL-1ɑ and IL-6 was even more effective at reducing the magnitude and duration of CFA-induced heat hypersensitivity. Our findings demonstrate a functional link between Ca V 2.2 channel activity and the release of IL-6 in the skin and show that Ca V 2.2 channels have a privileged role in the induction and maintenance of heat hypersensitivity during chronic forms of neuroinflammation in the skin.

  PublisherOA PDFDOI

• Machine Learning-Assisted Near-Infrared Spectral Fingerprinting for Macrophage Phenotyping

  ACS Nano · 2024-08-16 · 16 citations

  articleOpen access

  Spectral fingerprinting has emerged as a powerful tool that is adept at identifying chemical compounds and deciphering complex interactions within cells and engineered nanomaterials. Using near-infrared (NIR) fluorescence spectral fingerprinting coupled with machine learning techniques, we uncover complex interactions between DNA-functionalized single-walled carbon nanotubes (DNA-SWCNTs) and live macrophage cells, enabling in situ phenotype discrimination. Utilizing Raman microscopy, we showcase statistically higher DNA-SWCNT uptake and a significantly lower defect ratio in M1 macrophages compared to M2 and naive phenotypes. NIR fluorescence data also indicate that distinctive intraendosomal environments of these cell types give rise to significant differences in many optical features, such as emission peak intensities, center wavelengths, and peak intensity ratios. Such features serve as distinctive markers for identifying different macrophage phenotypes. We further use a support vector machine (SVM) model trained on SWCNT fluorescence data to identify M1 and M2 macrophages, achieving an impressive accuracy of >95%. Finally, we observe that the stability of DNA-SWCNT complexes, influenced by DNA sequence length, is a crucial consideration for applications, such as cell phenotyping or mapping intraendosomal microenvironments using AI techniques. Our findings suggest that shorter DNA-sequences like GT6 give rise to more improved model accuracy (>87%) due to increased active interactions of SWCNTs with biomolecules in the endosomal microenvironment. Implications of this research extend to the development of nanomaterial-based platforms for cellular identification, holding promise for potential applications in real time monitoring of in vivo cellular differentiation.

  PublisherOA PDFDOI

• Peripheral Ca _V 2.2 channels in skin regulate prolonged heat hypersensitivity during neuroinflammation

  bioRxiv (Cold Spring Harbor Laboratory) · 2024-07-17 · 1 citations

  preprintOpen access

  Abstract Neuroinflammation can lead to chronic maladaptive pain affecting millions of people worldwide. Neurotransmitters, cytokines, and ion channels are implicated in neuro-immune cell signaling but their roles in specific behavioral responses are not fully elucidated. Voltage-gated Ca V 2.2 channel activity in skin controls rapid and transient heat hypersensitivity induced by intradermal capsaicin via IL-1α cytokine signaling. Ca V 2.2 channels are not, however, involved in mechanical hypersensitivity that developed in the same animal model. Here, we show that Ca V 2.2 channels are also critical for heat hypersensitivity induced by the intradermal ( id ) Complete Freund’s Adjuvant (CFA) model of chronic neuroinflammation that involves ongoing cytokine signaling for days. Ongoing CFA-induced cytokine signaling cascades in skin lead to pronounced edema, and hypersensitivity to sensory stimuli. Peripheral Ca V 2.2 channel activity in skin is required for the full development and week-long time course of heat hypersensitivity induced by id CFA. Ca V 2.2 channels, by contrast, are not involved in paw edema and mechanical hypersensitivity. CFA induced increases in cytokines in hind paws including IL-6 which was dependent on Ca V 2.2 channel activity. Using IL-6 specific neutralizing antibodies, we show that IL-6 contributes to heat hypersensitivity and, neutralizing both IL-1α and IL-6 was even more effective at reducing the magnitude and duration of CFA-induced heat hypersensitivity. Our findings demonstrate a functional link between Ca V 2.2 channel activity and the release of IL-6 in skin and show that Ca V 2.2 channels have a privileged role in the induction and maintenance of heat hypersensitivity during chronic forms of neuroinflammation in skin. Significance Statement Neuroinflammation can lead to chronic maladaptive pain. Neurotransmitters, ion channels, cytokines, and cytokine receptors are implicated in neuron-immune signaling, but their importance in mediating specific behavioral responses are not fully elucidated. We show that the activity of peripheral Ca V 2.2 calcium ion channels in skin play a unique role in the induction and maintenance of heat hypersensitivity in the CFA model of prolonged neuroinflammation, without accompanying effects on edema and mechanical hypersensitivity. Blocking peripheral Ca V 2.2 channel activity reduces local cytokine levels in hind paws injected with CFA including IL-6 and neutralizing IL-6 reduces CFA- induced heat hypersensitivity. Our studies define key signaling molecules that act locally in skin to trigger and maintain heat hypersensitivity during chronic neuroinflammation.

  PublisherDOI

• Aspartic proteases are abundant and active in acidified wound fluid

  bioRxiv (Cold Spring Harbor Laboratory) · 2024-06-30 · 1 citations

  preprintOpen access

  Abstract Wound healing necessitates a balance between synthesis and breakdown of extracellular matrix components, which is tightly regulated by proteases and their inhibitors. Studies have shown that treatment of poorly healing wounds with acid results in improved healing. In this study, we systematically evaluated changes in proteolytic activity of murine wound fluid upon acidification. A library of 228 synthetic peptides served as reporters of protease activity at pH 7.4, pH 5.0 and pH 3.5. The peptide digestion patterns differed at each pH, revealing that proteases active at pH 7.4 are inactivated at pH 3.5. Notably, aspartic acid proteases emerged as the dominant active enzymes at pH 3.5 and their activity was inhibited by pepstatin. Using a fluorogenic substrate, we quantified aspartic protease activity across varying pH levels and demonstrated optimal activity between pH 3.0 and 3.8. This activity was detectable as early as one day post-injury and persisted over the following ten days. Importantly, human wound fluid exhibited the same activity profile, validating the mouse model as a relevant system for studying acid-mediated wound healing processes.

  PublisherOA PDFDOI

• Interleukin-1α links peripheral CaV2.2 channel activation to rapid adaptive increases in heat sensitivity in skin

  Scientific Reports · 2024-04-20 · 7 citations

  articleOpen access

  Abstract Neurons have the unique capacity to adapt output in response to changes in their environment. Within seconds, sensory nerve endings can become hypersensitive to stimuli in response to potentially damaging events. The underlying behavioral response is well studied, but several of the key signaling molecules that mediate sensory hypersensitivity remain unknown. We previously discovered that peripheral voltage-gated Ca V 2.2 channels in nerve endings in skin are essential for the rapid, transient increase in sensitivity to heat, but not to mechanical stimuli, that accompanies intradermal capsaicin. Here we report that the cytokine interleukin-1α (IL-1α), an alarmin, is necessary and sufficient to trigger rapid heat and mechanical hypersensitivity in skin. Of 20 cytokines screened, only IL-1α was consistently detected in hind paw interstitial fluid in response to intradermal capsaicin and, similar to behavioral sensitivity to heat, IL-1α levels were also dependent on peripheral Ca V 2.2 channel activity. Neutralizing IL-1α in skin significantly reduced capsaicin-induced changes in hind paw sensitivity to radiant heat and mechanical stimulation. Intradermal IL-1α enhances behavioral responses to stimuli and, in culture, IL-1α enhances the responsiveness of Trpv1 -expressing sensory neurons. Together, our data suggest that IL-1α is the key cytokine that underlies rapid and reversible neuroinflammatory responses in skin.

  PublisherOA PDFDOI

Recent grants

• BioMedical Big Data Core

  NIH · $45.2M · 2016–2026

• NIH Grant R01DK033365

  NIH · $754k · 1996

• Influence of the lung microbiome on macrophage responses to lung damage

  NIH · $2.4M · 2018–2024

Frequent coauthors

• Meredith J. Crane

  Brown University

  46 shared

• Thomas Decker

  Max Perutz Labs

  42 shared

• Pia Gamradt

  Université Claude Bernard Lyon 1

  36 shared

• John Blackwell

  30 shared

• Robert Simha

  Indian Institute of Technology Madras

  29 shared

• David H. Raulet

  University of California, Berkeley

  27 shared

• Jorge E. Albina

  Island Hospital

  25 shared

• Ethan S. FitzGerald

  Brown University

  16 shared

Labs

• Jamieson LabPI

  Lab 2023 (mostly all there)

Education

• Ph.D., MCB

  University of California Berkeley

  2003

• B.A.

  Carleton College

  1997