About

Dr. Matthew D. Koci is a Professor in the Prestage Department of Poultry Science at NC State University, specializing in immunology, virology, and host-pathogen interactions. He earned his Bachelor of Science degree in Biology from Virginia Polytechnic Institute and State University in 1997, followed by a Master of Science in Infectious Diseases and a Ph.D. in Pathology from the University of Georgia in 1999 and 2003, respectively. His research focuses on understanding how bacteria and viruses cause disease and how the host responds to these threats, with a particular emphasis on gut health and the communication between the intestinal microbiome and the mucosal immune system. His work aims to develop novel strategies for disease prevention and to promote health, welfare, and performance in animals. Dr. Koci's laboratory investigates immune mechanisms that enable animals to recognize, respond to, eliminate, and develop resistance to pathogens, analyzing both cellular and molecular aspects of the host response. His primary research projects include studying innate immune responses involved in astrovirus-induced gastroenteritis, understanding how genetic polymorphisms affect resistance to infection, and exploring how changes in the intestinal microflora influence gut physiology and overall animal health.

Research topics

• Cell biology
• Biology
• Immunology
• Ecology
• Biochemistry
• Engineering
• Microbiology
• Virology
• Genetics

Selected publications

• NF-κB activation enhances STING signaling by altering microtubule-mediated STING trafficking

  Cell Reports · 2025-12-19 · 1 citations

  erratumOpen access
  PublisherDOI

• LL-37 transports immunoreactive cGAMP to activate STING signaling and enhance interferon-mediated host antiviral immunity

  Cell Reports · 2025-12-01

  articleOpen access
  PublisherDOI

• Pleurotus eryngii polysaccharides alleviate aflatoxin B1-induced liver inflammation in ducks involving in remodeling gut microbiota and regulating SCFAs transport via the gut-liver axis

  International Journal of Biological Macromolecules · 2024-05-13 · 13 citations

  article
  PublisherDOI

• Widespread prevalence of plasmid-mediated blaCTX-M type extended-spectrum beta-lactamase Escherichia coli in backyard broiler production systems in the United States

  PLoS ONE · 2024-06-03 · 5 citations

  articleOpen accessCorresponding

  Extended-spectrum beta-lactamase (ESBL) Escherichia coli (E. coli) is an emerging pathogen of high concern given its resistance to extended-spectrum cephalosporins. Broiler chicken, which is the number one consumed meat in the United States and worldwide, can be a reservoir of ESBL E. coli. Backyard poultry ownership is on the rise in the United States, yet there is little research investigating prevalence of ESBL E. coli in this setting. This study aims to identify the prevalence and antimicrobial resistance profiles (phenotypically and genotypically) of ESBL E. coli in some backyard and commercial broiler farms in the U.S. For this study ten backyard and ten commercial farms were visited at three time-points across flock production. Fecal (n = 10), litter/compost (n = 5), soil (n = 5), and swabs of feeders and waterers (n = 6) were collected at each visit and processed for E. coli. Assessment of ESBL phenotype was determined through using disk diffusion with 3rd generation cephalosporins, cefotaxime and ceftazidime, and that with clavulanic acid. Broth microdilution and whole genome sequencing were used to investigate both phenotypic and genotypic resistance profiles, respectively. ESBL E. coli was more prevalent in backyard farms with 12.95% of samples testing positive whereas 0.77% of commercial farm samples were positive. All isolates contained a blaCTX-M gene, the dominant variant being blaCTX-M-1, and its presence was entirely due to plasmids. Our study confirms concerns of growing resistance to fourth generation cephalosporin, cefepime, as roughly half (51.4%) of all isolates were found to be susceptible dose-dependent and few were resistant. Resistance to non-beta lactams, gentamicin and ciprofloxacin, was also detected in our samples. Our study identifies prevalence of blaCTX-M type ESBL E. coli in U.S. backyard broiler farms, emphasizing the need for interventions for food and production safety.

  PublisherOA PDFDOI

• Rutin, a natural flavonoid glycoside, ameliorates zearalenone induced liver inflammation via inhibiting lipopolysaccharide gut leakage and NF-κB signaling pathway in mice

  Food and Chemical Toxicology · 2024-07-24 · 13 citations

  article
  PublisherDOI

• Fluoroquinolone-resistant <i>Campylobacter</i> in backyard and commercial broiler production systems in the United States

  JAC-Antimicrobial Resistance · 2024-07-03 · 8 citations

  articleOpen access

  Abstract Objectives Campylobacter spp. are one of the leading foodborne pathogens in the world, and chickens are a known reservoir. This is significant considering broiler chicken is the top consumed meat worldwide. In the USA, backyard poultry production is increasing, but little research has been done to investigate prevalence and antimicrobial resistance associated with Campylobacter in these environments. Methods Our study encompasses a farm-to-genome approach to identify Campylobacter and investigate its antimicrobial resistance phenotypically and genotypically. We travelled to 10 backyard and 10 integrated commercial broiler farms to follow a flock throughout production. We sampled at days 10, 31 and 52 for backyard and 10, 24 and 38 for commercial farms. Bird faecal (n = 10) and various environmental samples (soil n = 5, litter/compost n = 5, and feeder and waterer swabs n = 6) were collected at each visit and processed for Campylobacter. Results Our results show a higher prevalence of Campylobacter in samples from backyard farms (21.9%) compared to commercial (12.2%). Most of our isolates were identified as C. jejuni (70.8%) and the remainder as C. coli (29.2%). Antimicrobial susceptibility testing reveals phenotypic resistance to ciprofloxacin (40.2%), an important treatment drug for Campylobacter infection, and tetracycline (46.6%). A higher proportion of resistance was found in C. jejuni isolates and commercial farms. Whole-genome sequencing revealed resistance genes, such as tet(O) and gyrA_T86I point mutation, that may confer resistance. Conclusion Overall, our research emphasizes the need for interventions to curb prevalence of resistant Campylobacter spp. on broiler production systems.

  PublisherOA PDFDOI

• NF-κB activation enhances STING signaling by altering microtubule-mediated STING trafficking

  Cell Reports · 2023 · 166 citations

  • Cell biology
  • Biology
  • Genetics

  It is widely known that stimulator of interferon genes (STING) can trigger nuclear factor κB (NF-κB) signaling. However, whether and how the NF-κB pathway affects STING signaling remains largely unclear. Here, we report that Toll-like receptor (TLR)-, interleukin-1 receptor (IL-1R)-, tumor necrosis factor receptor (TNFR)-, growth factor receptor (GF-R)-, and protein kinase C (PKC)-mediated NF-κB signaling activation dramatically enhances STING-mediated immune responses. Mechanistically, we find that STING interacts with microtubules, which plays a crucial role in STING intracellular trafficking. We further uncover that activation of the canonical NF-κB pathway induces microtubule depolymerization, which inhibits STING trafficking to lysosomes for degradation. This leads to increased levels of activated STING that persist for a longer period of time. The synergy between NF-κB and STING triggers a cascade-amplified interferon response and robust host antiviral defense. In addition, we observe that several gain-of-function mutations of STING abolish the microtubule-STING interaction and cause abnormal STING trafficking and ligand-independent STING autoactivation. Collectively, our data demonstrate that NF-κB activation enhances STING signaling by regulating microtubule-mediated STING trafficking.

  PublisherOA PDFDOI

• Abstract 2661: Participants Gain Significant Professional Skills and Communication Confidence through the Art of Science Communication Course: A Retrospective Survey Study

  Journal of Biological Chemistry · 2023-01-01

  articleOpen access
  PublisherDOI

• Chlorogenic Acid Alleviated AFB1-Induced Hepatotoxicity by Regulating Mitochondrial Function, Activating Nrf2/HO-1, and Inhibiting Noncanonical NF-κB Signaling Pathway

  Antioxidants · 2023-11-22 · 31 citations

  articleOpen access

  Aflatoxin B1 (AFB1), a kind of mycotoxin, imposes acute or chronic toxicity on humans and causes great public health concerns. Chlorogenic acid (CGA), a natural phenolic substance, shows a powerful antioxidant and anti-inflammatory effect. This study was conducted to investigate the effect and mechanism of CGA on alleviating cytotoxicity induced by AFB1 in L-02 cells. The results showed that CGA (160 μM) significantly recovered cell viability and cell membrane integrity in AFB1-treated (8 μM) cells. Furthermore, it was found that CGA reduced AFB1-induced oxidative injury by neutralizing reactive oxygen species (ROS) and activating the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway. In addition, CGA showed anti-inflammatory effects as it suppressed the expression of inflammation-related genes (IL-6, IL-8, and TNF-α) and AFB1-induced noncanonical nuclear factor kappa-B (NF-κB) activation. Moreover, CGA mitigated AFB1-induced apoptosis by maintaining the mitochondrial membrane potential (MMP) and inhibiting mRNA expressions of Caspase-3, Caspase-8, Bax, and Bax/Bcl-2. These findings revealed a possible mechanism: CGA prevents AFB1-induced cytotoxicity by maintaining mitochondrial membrane potential, activating Nrf2/HO-1, and inhibiting the noncanonical NF-κB signaling pathway, which may provide a new direction for the application of CGA.

  PublisherOA PDFDOI

• Beyond Better Medicines

  2023-08-04

  preprintOpen access1st authorCorresponding

  In 50 years, what are you going to tell your grandkids about the COVID-19 pandemic? More importantly, what are you going to tell them about how you and your generation took the lessons from COVID-19 to make our society more resistant and resilient to disease? COVID-19 highlighted many of the inequities in our public health system; to solve these issues it's going to take everyone, not just those in healthcare and medical sciences. We need engineers, data scientists, policymakers, communicators, sociologists and artists. In short, we need contributors from all majors and disciplines to help ensure a future where everyone has the best chance at living a life free of disease.

  PublisherOA PDFDOI

Frequent coauthors

• Rizwana Ali

  North Carolina State University

  34 shared

• Stacey Schultz‐Cherry

  24 shared

• Hosni M. Hassan

  North Carolina State University

  16 shared

• Mary Mendoza

  North Carolina State University

  15 shared

• Anne Ballou

  14 shared

• Xubiao Wei

  State Key Laboratory of Animal Nutrition

  11 shared

• R. A. Ali

  Northwell Health

  9 shared

• Prashant K. Nighot

  Penn State Milton S. Hershey Medical Center

  8 shared

Labs

• Prestage Department of Poultry SciencePI

Education

• Ph.D., Pathology

  University of Georgia

  2003

• M.S., Infectious Diseases

  University of Georgia

  1999

• B.S. Biology microbiology/immunology option, Biology

  Virginia Polytechnic Institute and State University

  1997