Mark S. Smeltzer Institution-verified
Sourced from institutional research profiles (UAMS TRI or ARA).
Infectious Disease Research - UAMS Center for Microbial Pathogenesis and Host Inflammatory Responses
faculty
Microbiology & Immunology, College of Medicine
Research Areas
Biography and Research Information
OverviewAI-generated summary
Mark S. Smeltzer is a researcher at the University of Arkansas for Medical Sciences (UAMS) within the Infectious Disease Research division of the Center for Microbial Pathogenesis and Host Inflammatory Responses, and the Department of Microbiology & Immunology.
His research focuses on the pathogenesis of *Staphylococcus aureus* infections, particularly those involving biofilms. Smeltzer investigates the mechanisms by which *S. aureus* causes disease, including the role of virulence factors such as proteases. His work has explored the genetic regulation of these factors, including the impact of mutations in genes like *purR* and *sarA* on protease production and overall virulence. He has also examined host responses, such as osteoclast formation mediated by RANKL in the context of osteomyelitis.
Smeltzer's work has been supported by federal grants, and he has published extensively on these topics. His h-index is 54 with over 10,900 citations. He collaborates with several researchers at UAMS, including Karen E. Beenken and Mara J. Campbell, with whom he has co-authored numerous publications. Smeltzer leads a research group and maintains an active lab website.
Metrics
- h-index: 55
- Publications: 167
- Citations: 11,055
Selected Publications
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Lipolysis of host triacylglyceride-rich lipoproteins creates a toxic microenvironment for <i>Staphylococcus aureus</i> (2026)
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Staphylococcus aureus Biofilm-Associated Infections: Have We Found a Clinically Relevant Target? (2025)
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Staphylococcus aureus Proteins Implicated in the Reduced Virulence of sarA and sarA/agr Mutants in Osteomyelitis (2025)
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The ability of <i>sarA</i> to limit protease production plays a key role in the pathogenesis of <i>Staphylococcus aureus</i> osteomyelitis irrespective of the functional status of <i>agr</i> (2024)
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RANKL-mediated osteoclast formation is required for bone loss in a murine model of Staphylococcus aureus osteomyelitis (2024)
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Increased production of aureolysin and staphopain A is a primary determinant of the reduced virulence of <i>Staphylococcus aureus sarA</i> mutants in osteomyelitis (2024)
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Comparative evaluation of small molecules reported to be inhibitors of <i>Staphylococcus aureus</i> biofilm formation (2023)
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The major role of <i>sarA</i> in limiting <i>Staphylococcus aureus</i> extracellular protease production is correlated with decreased virulence in diverse clinical isolates in osteomyelitis (2022)
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Pyroptosis and pyroptosis-inducing cancer drugs (2022)
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Is amplification bias consequential in transposon sequencing (TnSeq) assays? A case study with a Staphylococcus aureus TnSeq library subjected to PCR-based and amplification-free enrichment methods (2021)
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Evaluation of a bone filler scaffold for local antibiotic delivery to prevent Staphylococcus aureus infection in a contaminated bone defect (2021)
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4-4-(Anilinomethyl)-3-[4-(trifluoromethyl)phenyl]-1H-pyrazol-1-ylbenzoic acid derivatives as potent anti-gram-positive bacterial agents (2021)
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Limiting protease production plays a key role in the pathogenesis of the divergent clinical isolates of <i>Staphylococcus aureus</i> LAC and UAMS-1 (2021)
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Evaluation of bone and kidney toxicity of BT2-peg2, a potential carrier for the targeted delivery of antibiotics to bone (2021)
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The Increased Accumulation of Staphylococcus aureus Virulence Factors Is Maximized in a <i>purR</i> Mutant by the Increased Production of SarA and Decreased Production of Extracellular Proteases (2021)
ARA Academy 2017 ARA Fellow
Dr. Smeltzer dedicates his research to combating Staphylococcus aureus, a bacterial pathogen responsible for approximately 20,000 American deaths annually. He focuses on bone infections and those involving indwelling orthopaedic devices. He also serves as Program Director of a COBRE promoting infectious disease research capacity at UAMS and central Arkansas.
Policy Impact
Leads a COBRE center promoting infectious disease research capacity in central Arkansas, generating NIH institutional funding and training biomedical researchers.
Growth Areas
['Population Health Innovations & Clinical Research']
Federal Grants 3 $1,777,311 total
Center for Microbial Pathogenesis and Host Inflammatory Responses
Research Interests
Staphylococcus aureus, Staphylococcal infection, Osteomyelitis, Biofilm, Regulation
Grants & Funding
- sarA as a Target for the Treatment and Prevention of Staphylococcal Biofilm-Associated Infection US Department of the Army Principal Investigator
- sar-mediated regulation in Staphylococcus aureus NIH Principal Investigator
- Capsule regulatory network in S. aureus pathogenesis NIH Co-Investigator
- Center for Microbial Pathogenesis and Host Inflammatory Responses NIH Principal Investigator
- Biofilm Dissemination in Staphylococcus aureus NIH/Nat. Inst. of Allergy & Infectious Diseases - Pass Through: University of Southern Mississippi Principal Investigator
- Center for Microbial Pathogenesis and Host Inflammatory Responses NIH/Nat. Inst. of General Medical Sciences Principal Investigator
- Investigating a Flexible, Degradable Local Antimicrobial Delivery System - Continuation - Continuation DHHS - Biomedical Advanced Research and Development Authority - Pass Through: University of Memphis Principal Investigator
- Chitosan films for prevention of wound infections US Department of the Army Principal Investigator
Collaboration Network
Top Collaborators
- Evaluation of a bone filler scaffold for local antibiotic delivery to prevent Staphylococcus aureus infection in a contaminated bone defect
- Limiting protease production plays a key role in the pathogenesis of the divergent clinical isolates of <i>Staphylococcus aureus</i> LAC and UAMS-1
- RANKL-mediated osteoclast formation is required for bone loss in a murine model of Staphylococcus aureus osteomyelitis
- The major role of <i>sarA</i> in limiting <i>Staphylococcus aureus</i> extracellular protease production <i>in vitro</i> is correlated with decreased virulence in diverse clinical isolates in osteomyelitis
- The Increased Accumulation of Staphylococcus aureus Virulence Factors Is Maximized in a <i>purR</i> Mutant by the Increased Production of SarA and Decreased Production of Extracellular Proteases
Showing 5 of 14 shared publications
- Evaluation of a bone filler scaffold for local antibiotic delivery to prevent Staphylococcus aureus infection in a contaminated bone defect
- RANKL-mediated osteoclast formation is required for bone loss in a murine model of Staphylococcus aureus osteomyelitis
- The major role of <i>sarA</i> in limiting <i>Staphylococcus aureus</i> extracellular protease production <i>in vitro</i> is correlated with decreased virulence in diverse clinical isolates in osteomyelitis
- Increased production of aureolysin and staphopain A is a primary determinant of the reduced virulence of <i>Staphylococcus aureus sarA</i> mutants in osteomyelitis
- The ability of <i>sarA</i> to limit protease production plays a key role in the pathogenesis of <i>Staphylococcus aureus</i> osteomyelitis irrespective of the functional status of <i>agr</i>
Showing 5 of 10 shared publications
- Evaluation of a bone filler scaffold for local antibiotic delivery to prevent Staphylococcus aureus infection in a contaminated bone defect
- Limiting protease production plays a key role in the pathogenesis of the divergent clinical isolates of <i>Staphylococcus aureus</i> LAC and UAMS-1
- The major role of <i>sarA</i> in limiting <i>Staphylococcus aureus</i> extracellular protease production <i>in vitro</i> is correlated with decreased virulence in diverse clinical isolates in osteomyelitis
- The Increased Accumulation of Staphylococcus aureus Virulence Factors Is Maximized in a <i>purR</i> Mutant by the Increased Production of SarA and Decreased Production of Extracellular Proteases
- Increased production of aureolysin and staphopain A is a primary determinant of the reduced virulence of <i>Staphylococcus aureus sarA</i> mutants in osteomyelitis
Showing 5 of 7 shared publications
- Staphylococcal infection prevention using antibiotic‐loaded mannitol–chitosan paste in a rabbit model of implant‐associated osteomyelitis
- Biofilm-biomaterial interactions: understanding, preventing, and eradicating attachment in infection
- The Increased Accumulation of Staphylococcus aureus Virulence Factors Is Maximized in a <i>purR</i> Mutant by the Increased Production of SarA and Decreased Production of Extracellular Proteases
- Is amplification bias consequential in transposon sequencing (TnSeq) assays? A case study with a Staphylococcus aureus TnSeq library subjected to PCR-based and amplification-free enrichment methods
- The Increased Accumulation of Staphylococcus aureus Virulence Factors Is Maximized in a <i>purR</i> Mutant by the Increased Production of SarA and Decreased Production of Extracellular Proteases
- Is amplification bias consequential in transposon sequencing (TnSeq) assays? A case study with a Staphylococcus aureus TnSeq library subjected to PCR-based and amplification-free enrichment methods
- The Increased Accumulation of Staphylococcus aureus Virulence Factors Is Maximized in a <i>purR</i> Mutant by the Increased Production of SarA and Decreased Production of Extracellular Proteases
- Comparative evaluation of small molecules reported to be inhibitors of <i>Staphylococcus aureus</i> biofilm formation
- Evaluation of a bone filler scaffold for local antibiotic delivery to prevent Staphylococcus aureus infection in a contaminated bone defect
- Limiting protease production plays a key role in the pathogenesis of the divergent clinical isolates of <i>Staphylococcus aureus</i> LAC and UAMS-1
- Staphylococcal infection prevention using antibiotic‐loaded mannitol–chitosan paste in a rabbit model of implant‐associated osteomyelitis
- Staphylococcal infection prevention using antibiotic‐loaded mannitol–chitosan paste in a rabbit model of implant‐associated osteomyelitis
- Staphylococcal infection prevention using antibiotic‐loaded mannitol–chitosan paste in a rabbit model of implant‐associated osteomyelitis
- Staphylococcal infection prevention using antibiotic‐loaded mannitol–chitosan paste in a rabbit model of implant‐associated osteomyelitis
- Staphylococcal infection prevention using antibiotic‐loaded mannitol–chitosan paste in a rabbit model of implant‐associated osteomyelitis
- Evaluation of bone and kidney toxicity of BT2-peg2, a potential carrier for the targeted delivery of antibiotics to bone
- Evaluation of bone and kidney toxicity of BT2-peg2, a potential carrier for the targeted delivery of antibiotics to bone
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