Julia L M Dunn1, Rebecca A Hunter2, Karli Gast3, Robert Maile4, Bruce A Cairns5, Mark H Schoenfisch6. 1. Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, NC 27599, United States. Electronic address: jlmalik@email.unc.edu. 2. Department of Chemistry, University of North Carolina, Chapel Hill, NC 27599, United States. Electronic address: rahunter@unc.edu. 3. Department of Chemistry, University of North Carolina, Chapel Hill, NC 27599, United States. Electronic address: karli_gast@med.unc.edu. 4. Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, NC 27599, United States; North Carolina Jaycee Burn Center, Department of Surgery, University of North Carolina, Chapel Hill, NC 27599, United States. Electronic address: robmaile@med.unc.edu. 5. Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, NC 27599, United States; North Carolina Jaycee Burn Center, Department of Surgery, University of North Carolina, Chapel Hill, NC 27599, United States. Electronic address: bruce_cairns@med.unc.edu. 6. Department of Chemistry, University of North Carolina, Chapel Hill, NC 27599, United States. Electronic address: schoenfisch@unc.edu.
Abstract
PURPOSE: Burn is associated with severe immune dysfunction, including an anti-inflammatory state that occurs late after burn. While increased nitric oxide (NO) production is associated with severe infection and sepsis, the effect of burn trauma on these levels during a non-lethal infection remains unknown. We hypothesized that in a mouse model, (1) NO levels would be increased after infection without trauma and (2) burn would lead to decreased NO production even during infection. METHODS: Mice were infected via intra-tracheal inoculation with Pseudomonas aeruginosa 14 d following a 20% total body surface area contact burn. At 48h following infection, blood was drawn to quantify NO concentrations using a microfluidic electrochemical sensor. SIGNIFICANT FINDINGS: In uninjured mice, infection caused a significant increase in blood NO levels. Increases in NO occurred in a dose-dependent response to the bacterial inoculum. Following burn, an identical infection did not elicit increases in NO. CONCLUSIONS: While increases in NO are expected over the course of an infection without prior trauma, burn and subsequent immune suppression decreases NO levels even in the presence of infection.
PURPOSE: Burn is associated with severe immune dysfunction, including an anti-inflammatory state that occurs late after burn. While increased nitric oxide (NO) production is associated with severe infection and sepsis, the effect of burn trauma on these levels during a non-lethal infection remains unknown. We hypothesized that in a mouse model, (1) NO levels would be increased after infection without trauma and (2) burn would lead to decreased NO production even during infection. METHODS:Mice were infected via intra-tracheal inoculation with Pseudomonas aeruginosa 14 d following a 20% total body surface area contact burn. At 48h following infection, blood was drawn to quantify NO concentrations using a microfluidic electrochemical sensor. SIGNIFICANT FINDINGS: In uninjured mice, infection caused a significant increase in blood NO levels. Increases in NO occurred in a dose-dependent response to the bacterial inoculum. Following burn, an identical infection did not elicit increases in NO. CONCLUSIONS: While increases in NO are expected over the course of an infection without prior trauma, burn and subsequent immune suppression decreases NO levels even in the presence of infection.
Authors: Laurel B Kartchner; Cindy J Gode; Julia L M Dunn; Lindsey I Glenn; Danté N Duncan; Matthew C Wolfgang; Bruce A Cairns; Robert Maile Journal: Burns Date: 2019-03-02 Impact factor: 2.744
Authors: Julia L M Dunn; Laurel B Kartchner; Wesley H Stepp; Lindsey I Glenn; Madison M Malfitano; Samuel W Jones; Claire M Doerschuk; Robert Maile; Bruce A Cairns Journal: Am J Physiol Lung Cell Mol Physiol Date: 2018-01-25 Impact factor: 5.464
Authors: Cressida Mahung; Wesley H Stepp; Clayton Long; Madison Malfitano; Irmak Saklayici; Shannon M Wallet; Laura Y Zhou; Haibo Zhou; Bruce A Cairns; Robert Maile Journal: J Trauma Acute Care Surg Date: 2022-03-30 Impact factor: 3.697
Authors: Julia L M Dunn; Laurel B Kartchner; Karli Gast; Marci Sessions; Rebecca A Hunter; Lance Thurlow; Anthony Richardson; Mark Schoenfisch; Bruce A Cairns; Robert Maile Journal: J Leukoc Biol Date: 2018-02-02 Impact factor: 4.962
Authors: Hannah R Hall; Cressida Mahung; Julia L M Dunn; Laurel M Kartchner; Roland F Seim; Bruce A Cairns; Shannon M Wallet; Robert Maile Journal: Int J Mol Sci Date: 2022-08-07 Impact factor: 6.208
Authors: Micah L Willis; Cressida Mahung; Shannon M Wallet; Alexandra Barnett; Bruce A Cairns; Leon G Coleman; Robert Maile Journal: J Leukoc Biol Date: 2021-08-03 Impact factor: 4.962