Direct detection of blood nitric oxide reveals a burn-dependent decrease of nitric oxide in response to Pseudomonas aeruginosa infection.
OBJECTIVE
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.
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.
Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, NC 27599, United States. Electronic address: jlmalik@email.unc.edu.
Julia L M
JL
Dunn
Department of Chemistry, University of North Carolina, Chapel Hill, NC 27599, United States. Electronic address: rahunter@unc.edu.
Rebecca A
RA
Hunter
Department of Chemistry, University of North Carolina, Chapel Hill, NC 27599, United States. Electronic address: karli_gast@med.unc.edu.
Karli
K
Gast
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.
Robert
R
Maile
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.
Bruce A
BA
Cairns
Department of Chemistry, University of North Carolina, Chapel Hill, NC 27599, United States. Electronic address: schoenfisch@unc.edu.
Mark H
MH
Schoenfisch
D000818:Animals; D002056:Burns / Q000097:blood*; D004195:Disease Models, Animal; D005260:Female; D051379:Mice; D008810:Mice, Inbred C57BL; D009569:Nitric Oxide / Q000097:blood*; D018410:Pneumonia, Bacterial / Q000097:blood; D011552:Pseudomonas Infections / Q000097:blood*; D011550:Pseudomonas aeruginosa; D018805:Sepsis / Q000097:blood*
D009569:Nitric Oxide
Burn; Compensatory anti-inflammatory response syndrome; Electrochemistry; Microfluidic sensor; Nitric oxide; Pneumonia; Pseudomonas aeruginosa; Sepsis