Circulating Fibronectin Depletion in Burned Patients: Relationship to Development of Infection and Prognostic Value

Konter-Thioulouse, Elisabeth; Wassermann, D.; Ekindjian, Ohvanesse G.; Lebreton, F; Marien, M.; Schlotterer, M; Yonger, J

doi:10.1097/00004630-198511000-00004

Cited by 2 publications

(4 citation statements)

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“…to some degree above the sham, as is noted to occur following burn injury (Onarheim et al, 1991(Onarheim et al, , 1992Lantos et al, 2010;Rani et al, 2017). In contrast, FBN has been shown to have the opposite effect, as compared to HMGB-1 and HYL, with levels initially decreasing post-burn and then returning to normal over the proceeding days (Lanser et al, 1980;Grzybowski et al, 1983;Konter-Thioulouse et al, 1985;Sheng et al, 1987;Thompson et al, 1989). A similar trend was seen in our rat model, with recovery of FBN levels around POD 7.…”

Section: Discussionsupporting

confidence: 79%

“…Furthermore, while FBN showed initial recovery to sham levels, infectious groups began to show signs of decline by POD 11, in the case of FT burn. Although the change is minor here, it may still be relevant as it has been noted to occur in burn patients facing infection (Lanser et al, 1980;Konter-Thioulouse et al, 1985;Sheng et al, 1987;Koenig et al, 1988). Overall, the impact of infection leads to sequelae of the burn injury, whereby causing a greater host response compared to burn alone.…”

Section: Discussionmentioning

confidence: 93%

“…Aside from cellular and cytokine changes, DAMPs are also well-known to result from any traumatic injury, and act as triggers to the host's innate immune machineries, which potentially can lead to subsequent adaptive immune responses. The damage associated with burn and inflammation results in DAMPs being flushed into the system from the wound, which can include HMGB-1 (Lantos et al, 2010;Huang et al, 2011), HYL (Scheibner et al, 2006), and FBN (Konter-Thioulouse et al, 1985;Sheng et al, 1987). HMGB-1 is a nuclear protein that is typically secreted by macrophages at the site of injury to attract other immune cells; however, following injury it can also be released passively by damaged/necrotic cells, such as neutrophils (Scaffidi et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, HMGB-1 has been positively correlated with percent TBSA, to be higher in non-surviving burn patients, and elevated in those suffering from sepsis (Lantos et al, 2010;Huang et al, 2011). HYL and FBN are both extracellular matrix components present in the skin, which are dynamically altered following tissue damage in burn patients (Konter-Thioulouse et al, 1985;Sheng et al, 1987;Onarheim et al, 1992;Scheibner et al, 2006). HYL specifically is known to fragment following burn injury and ultimately increases at systemic levels.…”

Section: Discussionmentioning

confidence: 99%

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Comparative Analysis of the Host Response in a Rat Model of Deep-Partial and Full-Thickness Burn Wounds With Pseudomonas aeruginosa Infection

Weaver

Brandenburg

Smith

et al. 2020

Front. Cell. Infect. Microbiol.

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Burn wound injury affects soldiers and civilians alike, often resulting in a dynamic, but un-orchestrated, host response that can lead to infection, scarring, and potentially death. To mitigate these factors, it is important to have a clinically relevant model of burn wound infection that can be utilized for advancing burn wound treatments. Our previous reports have demonstrated the ability of Pseudomonas aeruginosa to generate a biofilm infection within a modified Walker-Mason rat burn model of deep-partial (DPT) and full-thickness (FT) burn wounds (10% total body surface area) in male Sprague-Dawley rats (350-450 g). Here, we further define this model with respect to the host response when challenged with P. aeruginosa infection between the two burn types. Following burn injury and immediate surface exposure to P. aeruginosa, inflammation at the local and systemic levels were monitored for an 11 days period. Compared to burn-only groups, infection with P. aeruginosa further promoted local inflammation in both DPT and FT burn wounds, which was evident by enhanced cellular influx (including neutrophils and monocytes), increased levels of several pro-inflammatory cytokines (IL-1β, IL-6, GRO/KC, andMIP-1α), and reduced IL-10. Systemically, only minor changes were seen in circulating white blood cells and cytokines; however, increases in high mobility group box-1 (HMGB-1) and hyaluronan, as well as decreases in fibronectin were noted particularly in FT burns. Compared to the burn-only group, P. aeruginosa infection resulted in sustained and/or higher levels of HMGB-1 and hyaluronan. Combined with our previous work that defined the burn depth and development of P. aeruginosa biofilms within the wound, this study further establishes this model by defining the host response to the burn and biofilm-infection. Furthermore, this characterization shows several similarities to what is clinically seen and establishes this model for future use in the development and testing of novel therapeutics for burn wound treatment at home and on the battlefield.

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