About

Michael Silverman, MD, PhD, is an Assistant Professor of Pediatrics (Infectious Diseases) at the Perelman School of Medicine at the University of Pennsylvania. He is also the Associate Director of the Pediatric Infectious Disease Fellowship at the Children's Hospital of Philadelphia and serves as the Director of Immunology at the Microbial Medicine Center at the same hospital. His educational background includes a BS in Biology from Cornell University (1998) and an MD, PhD in Medicine and Immunology from the University of Pennsylvania School of Medicine (2007). His clinical expertise focuses on immunocompromised patients, and his research interests encompass microbiome, immunology, HLA, MHC, antibiotics, the intestinal immune system, autoimmune diseases such as type I diabetes, IgA deficiency, and early life immune system development.

Research topics

• Biology
• Microbiology
• Genetics
• Immunology

Selected publications

• Hospice Choice (HC): A diet model for providing nutrition for inpatient hospice patients

  Journal of Pain and Symptom Management · 2026-05-12

  article
  PublisherDOI

• Joint profiling of gene expression and chromatin accessibility in pancreatic lymph nodes and spleens in human type 1 diabetes

  Science Immunology · 2025-11-21 · 2 citations

  articleOpen access

  Type 1 diabetes (T1D) is an autoimmune disease characterized by the destruction of insulin-producing β cells in the pancreas. While current therapies focus on managing the disease, a deeper understanding of the underlying molecular mechanisms is crucial for developing disease-modifying interventions. In this study, we conducted a comprehensive analysis of gene expression and chromatin accessibility in nearly 1 million immune cells from the pancreatic lymph nodes and spleens of 43 individuals with and without T1D. We found a distinct subset of CD4 T cells specifically present in the pancreatic lymph nodes of organ donors representing the active disease stage. These cells exhibited elevated activity of NFKB1 and BACH2 , along with extensive chromatin remodeling associated with these transcription factors, which we also corroborated in a mouse model of T1D. A better understanding of these NFKB1-BACH2 –expressing CD4 T cells may lead to therapeutic avenues for preventing or delaying T1D onset.

  PublisherOA PDFDOI

• Microbial succession at weaning is guided by microbial metabolism of host glycans

  Microbiome · 2025-10-28 · 1 citations

  articleOpen accessSenior author

  BACKGROUND: The weaning transition from a milk-based to a solid-food diet supports critical developmental changes to the intestinal microbiota and immune system. However, the specific microbial and host features that influence microbial succession at weaning are not well understood. RESULTS: Here, we developed a simple approach to investigate the complex dynamics of microbial succession during weaning by co-housing gnotobiotic mice colonized with the defined pre-weaning community PedsCom and the adult-derived consortium Oligo-MM12 (OMM12). Co-housing PedsCom mice with OMM12 recapitulated microbial succession at weaning and induced immune system maturation in PedsCom mice. Unexpectedly, we found that the OMM12 microbes with the highest host glycan utilization profiles were the most adept colonizers of PedsCom mice. Genomic analysis confirmed that PedsCom is deficient in the carbohydrate-active enzymes responsible for degrading host-derived glycans, including mucins, compared to adult-derived consortia. We validated a role for glycan utilization in vivo by demonstrating that the mucus-degrading commensal microbe Akkermansia muciniphila critically depends on the metabolism of mucin glycans for stable colonization of PedsCom mice. CONCLUSIONS: These findings highlight the importance of host-derived glycans in shaping microbial communities during the weaning transition and suggest host glycans as novel targets to modulate intestinal microbial populations, introduce beneficial probiotics, and enhance immune system development during weaning. Video Abstract.

  PublisherOA PDFDOI

• Microbial succession at weaning is guided by microbial metabolism of host glycans

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-02-20 · 1 citations

  preprintOpen accessSenior authorCorresponding

  Abstract The weaning transition from a milk-based to a solid-food diet supports critical developmental changes to the intestinal microbiome and immune system. However, the specific microbial and host features that influence microbial succession at weaning are not well understood. Here, we developed a simple approach to investigate the complex dynamics of microbial succession during weaning by co-housing gnotobiotic mice colonized with the defined pre-weaning community PedsCom and the adult-derived consortium OMM12. As expected, co-housing PedsCom mice with OMM12 recapitulated microbial succession at weaning and induced immune system maturation in PedsCom mice. Unexpectedly, we found that the OMM12 microbes with the highest host glycan utilization profiles were the most adept colonizers of PedsCom mice. Genomic analysis confirmed that PedsCom is deficient in the carbohydrate-active enzymes responsible for degrading host-derived glycans, including mucins, compared to adult-derived consortia. We validated a role for glycan utilization in vivo by demonstrating that the mucus-degrading commensal microbe Akkermansia muciniphila critically depends on the metabolism of mucin glycans for colonization of PedsCom mice. These findings highlight the importance of host-derived glycans in shaping microbial communities during the weaning transition and suggest host glycans as novel targets to modulate intestinal microbial populations, introduce beneficial probiotics, and enhance immune system development during weaning.

  PublisherDOI

• Setting the table for immune tolerance

  Science · 2025-08-14

  letter1st authorCorresponding

  Interaction between breast milk antibodies and gut microbes shape immune responses during weaning.

  PublisherDOI

• Human milk as a microbial pacemaker

  Cell Host & Microbe · 2025-06-01 · 3 citations

  articleSenior author
  PublisherDOI

• PLUGGING THE LEAK: A CASE OF SUCCESSFUL PLUG CLOSURE OF PERFORATED ANTERIOR MITRAL VALVE LEAFLET WITH AMPLATZER OCCLUDER DEVICE

  Journal of the American College of Cardiology · 2025-03-30

  articleOpen access
  PublisherDOI

• Single-cell quantification of the microbiota by flow cytometry: MicFLY

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-09-19

  preprintOpen access

  SUMMARY The intestinal microbiota regulates multiple host functions, including digestion and immune development. Our knowledge of the microbiota has been shaped by available technology that primarily measures relative abundance. However, understanding the basis of shifts in microbiota composition requires single cell, absolute abundance measurements. In response to this problem, we developed Mic robiota Fl ow C y tometry (MicFLY), a single cell technology that directly quantifies and characterizes total bacterial abundances with species-level resolution in the microbiota. Using MicFLY, we can identify all major intestinal taxa, discriminate live from dead bacteria, perform single cell measurements of heterogeneous bacterial mRNA expression and concurrently quantify Immunoglobulin (Ig) A and G binding to intestinal bacteria. Using longitudinal species-resolved, quantitative analysis of the preterm infant microbiota, we identify that E. coli unbound by IgG and IgA associates with the development of necrotizing enterocolitis. The application of MicFLY single cell technology permits measurement of the microbiota at a finer scale and with deeper mechanistic understanding of compositional changes.

  PublisherOA PDFDOI

• A lack of commensal microbiota influences the male reproductive tract intergenerationally in mice

  Reproduction · 2025-02-13 · 3 citations

  articleOpen access

  In brief: Germ-free mice display epididymal transcriptomic changes that were also evident in their conventionalized male offspring and mice lacking T and B cells. This paper demonstrates the role of microbiota and immune cells in the epididymis. Abstract: The microbiome encompasses the array of microorganisms inhabiting various niches in the body and is necessary for numerous physiological processes, including normal metabolism and a functioning immune system. Not only does the absence of a microbiome in mice impact the exposed animals but also inherited phenotypes in successive generations of progeny, suggesting that the absence of a microbiome impacts the germline and gametes. Indeed, recent research has identified a role of the gut microbiome in contributing to male fertility, in both healthy and disease states. While this link is beginning to be established, the impact of the microbiome on the male reproductive tract remains understudied. Here, we utilized a germ-free mouse model to examine the influence of the absence of microbes on the male reproductive tract. In contrast to mice with an established microbiome, germ-free mice display decreased testicular weight and the prevalence of an epididymitis-like inflammation phenotype. These histopathological changes are accompanied by transcriptomic dysregulation in the reproductive tract of germ-free mice, particularly in the cauda epididymis. Moreover, these transcriptomic changes are transmitted to the next generation with high correlation of gene expression in the cauda epididymis between germ-free mice and their conventionalized (microbiome-restored) male offspring, when compared to control mice. Ultimately, our findings identify the reproductive sequalae of males without a functional microbiome and additionally in their conventionalized offspring, suggesting that the paternal microbiota is an underappreciated contributor to male reproductive function.

  PublisherDOI

• Training the modern sports cardiologist: Designing a fellowship curriculum for a growing subspecialty

  American Journal of Preventive Cardiology · 2025-11-20

  articleOpen access

  Background: Sports cardiology is a rapidly evolving subspecialty addressing the prevention, evaluation, and management of cardiovascular disease in athletes and highly active individuals. Despite rising demand, no Accreditation Council for Graduate Medical Education (ACGME)-accredited fellowship exists, resulting in limited and inconsistent training pathways. Objective: We describe the development of a nonstandard training (NST) fellowship curriculum in sports cardiology at our institution, outlining its rationale, structure, and competencies to provide a potential model for other programs. Methods: Guided by American College of Cardiology (ACC) and European Society of Cardiology (ESC) frameworks, we designed a curriculum integrated into the third year of general cardiology fellowship. Core elements include structured clinical rotations, didactic teaching, case-based learning, pre-participation screenings, and scholarly activities. A multidisciplinary consortium of regional cardiologists was formed to expand clinical exposure and mentorship opportunities. Results: The curriculum emphasizes key competencies: pre-participation screening, distinguishing exercise-induced cardiac remodeling from pathology, management of symptomatic or diagnosed athletes, and shared decision-making. Clinical experiences are complemented by formal educational sessions, research opportunities, and collaborative conferences. Conclusion: A rigorous, competency-based NST fellowship in sports cardiology is feasible within existing fellowship structures. Our model may serve as a framework for institutions seeking to formalize training in this emerging subspecialty.

  PublisherDOI

Recent grants

• Transfer: Dissecting the interplay of MHC/HLA loci, the microbiota and autoimmune diabetes

  NIH · $893k · 2015–2020

Frequent coauthors

• Adam G. Golden

  University of Central Florida

  69 shared

• Paul J. Planet

  Children's Hospital of Philadelphia

  44 shared

• Jamal Green

  Children's Hospital of Philadelphia

  33 shared

• Jean‐Bernard Lubin

  Children's Hospital of Philadelphia

  30 shared

• S. Barry Issenberg

  Bond University

  26 shared

• Gary A. Koretzky

  Weill Cornell Medicine

  25 shared

• Tereza Duranova

  Children's Hospital of Philadelphia

  22 shared

• Maria D. Llorente

  Georgetown University

  20 shared

Labs

• Michael Silverman LabPI