Gut Microbial Changes and their Contribution to Post-Burn Pathology

Abstract

Burn injuries are a common form of traumatic injury that leads to significant morbidity and mortality worldwide. Burn injuries are characterized by inflammatory processes and alterations in numerous organ systems and functions. Recently, it has become apparent that the gastrointestinal bacterial microbiome is a key component of regulating the immune response and recovery from burn and can also contribute to significant detrimental sequelae after injury, such as sepsis and multiple organ failure. Microbial dysbiosis has been linked to multiple disease states; however, its role in exacerbating acute traumatic injuries, such as burn, is poorly understood. In this article, we review studies that document changes in the intestinal microbiome after burn injury, assess the implications in post-burn pathogenesis, and the potential for further discovery and research.

Alcohol use disorder as a potential risk factor forCOVID‐19 severity: A narrative review

“…Alcohol misuse associated with burn or trauma injury has been extensively researched and is associated with increased complications including lung inflammation, injury and death and susceptibility to infection and AUD patients require more resuscitation and have a longer hospital stay (Khair et al, 2022; Silver et al, 2008; Yeligar et al, 2016). Alcohol exacerbates posttrauma or burn levels of inflammatory cytokines especially IL‐1β, IL‐6 and TNF‐α production by monocytes and other immune cells (Luck et al, 2021; Szabo & Saha, 2015). As in COVID‐19, elevated levels of these 3 cytokines correlates with mortality in AUD burn patients and blocking IL‐6 is especially associated with decreased mortality in these patients (Chen et al, 2013; Paniri & Akhavan‐Niaki, 2020).…”

“…As in COVID‐19, elevated levels of these 3 cytokines correlates with mortality in AUD burn patients and blocking IL‐6 is especially associated with decreased mortality in these patients (Chen et al, 2013; Paniri & Akhavan‐Niaki, 2020). In addition, a major mechanism for alcohol proinflammatory effects is through exacerbating lung inflammation and injury through the gut‐liver‐lung axis leading to greater translocation of gut bacteria and bacterial products, such as lipopolysaccharide (LPS), into the lymphatic and portal blood which can drive systemic and liver, and lung, and activation of the NLRP3 inflammasome as in ARDS (Choudhry et al, 2004; Luck et al, 2021).…”

Machine learning links different gene patterns of viral infection to immunosuppression and immune-related biomarkers in severe burns

“…First, burns can lead to severe dysbiosis of the intestinal microbiota, reducing beneficial bacteria and increasing opportunistic pathogens ( 32 ). Secondly, the function of the intestinal mucosal barrier was damaged after burns, and bacteria invaded the blood from the intestine to induce sepsis ( 33 ). CMV latency occurs within the bone marrow, mainly within the monocyte/granulocyte progenitor cells ( 34 ), and the rate of CMV reactivation in burn patients varies from 55% to 71% ( 35 ).…”

Gastrointestinal dysfunction is associated with mortality in severe burn patients: a 10-year retrospective observational study from South China

“…Gut-related sepsis and MODS can still ensue even when the early associated GI dysfunction is relatively mild and reversible. These effects may be related to a dysbiosis with overgrowth of harmful bacteria due to the breakdown of the normal intestinal barrier and/or altered immune responsiveness [ 24 , 25 ]. Moreover, the role of selective decontamination of the bowel or the use of pre- or pro-biotics and their effects on mucosal immunology and clinical outcomes in critical burn patients are yet to be adequately determined [ 26 , 27 ].…”