The ecological community of microorganisms in/on humans, termed the microbiome, is vital for sustaining homeostasis. While culture-independent techniques have revealed the role of the gut microbiome in human health and disease, the role of the cutaneous microbiome in wound healing is less defined. Skin commensals are essential in the maintenance of the epithelial barrier function, regulation of the host immune system, and protection from invading pathogenic microorganisms. In this review, we summarize the literature derived from pre-clinical and clinical studies on how changes in the microbiome of various acute and chronic skin wounds impact wound healing tissue regeneration. Furthermore, we review the mechanistic insights garnered from model wound healing systems. Finally, in the face of growing concern about antibiotic-resistance, we will discuss alternative strategies for the treatment of infected wounds to improve wound healing and outcomes. Taken together, it has become apparent that commensals, symbionts, and pathogens on human skin have an intimate role in the inflammatory response that highlights several potential strategies to treat infected, non-healing wounds. Despite these promising results, there are some contradictory and controversial findings from existing studies and more research is needed to define the role of the human skin microbiome in acute and chronic wound healing.

The gut microbiome and its role in health and disease have recently been major focus areas of research. In this review, we summarize the different ways in which the gut microbiome interacts with the rest of the body, with focus areas on its relationships with immunity, the brain, and injury. The gut–brain axis, a communication network linking together the central and enteric nervous systems, represents a key bidirectional pathway with feed-forward and feedback mechanisms. The gut microbiota has a central role in this pathway and is significantly altered following injury, leading to a pro-inflammatory state within the central nervous system (CNS). Herein, we examine traumatic brain injury (TBI) in relation to this axis and explore potential interventions, which may serve as targets for improving clinical outcomes and preventing secondary brain injury.

BACKGROUND: Traumatic injury can lead to a compromised intestinal epithelial barrier, decreased gut perfusion, and inflammation. While recent studies indicate that the gut microbiome (GM) is altered early following traumatic injury, the impact of GM changes on clinical outcomes remains unknown. Our objective of this follow-up study was to determine if the GM is associated with clinical outcomes in critically injured patients. METHODS: We conducted a prospective, observational study in adult patients (N = 67) sustaining severe injury admitted to a level I trauma center. Fecal specimens were collected on admission to the emergency department, and microbial DNA from all samples was analyzed using the Quantitative Insights Into Microbial Ecology pipeline and compared against the Greengenes database. α-Diversity and β-diversity were estimated using the observed species metrics and analyzed with t tests and permutational analysis of variance for overall significance, with post hoc pairwise analyses. RESULTS: Our patient population consisted of 63% males with a mean age of 44 years. Seventy-eight percent of the patients suffered blunt trauma with 22% undergoing penetrating injuries. The mean body mass index was 26.9 kg/m². Significant differences in admission β-diversity were noted by hospital length of stay, intensive care unit hospital length of stay, number of days on the ventilator, infections, and acute respiratory distress syndrome (p < 0.05). β-Diversity on admission differed in patients who died compared with patients who lived (mean time to death, 8 days). There were also significantly less operational taxonomic units in samples from patients who died versus those who survived. A number of species were enriched in the GM of injured patients who died, which included some traditionally probiotic species such as Akkermansia muciniphilia, Oxalobacter formigenes, and Eubacterium biforme (p < 0.05). CONCLUSION: Gut microbiome diversity on admission in severely injured patients is predictive of a variety of clinically important outcomes. While our study does not address causality, the GM of trauma patients may provide valuable diagnostic and therapeutic targets for the care of injured patients. LEVEL OF EVIDENCE: Prognostic and epidemiological, level III.

Introduction: Severe trauma and hemorrhage in rats lead to changes in the beta diversity of the commensal bacteria found in the gut. Because short-chain fatty acids (SCFA) are produced by these bacteria, SCFA concentration may also change following trauma and hemorrhage and reflect these alterations in the microbiome. Objective: To determine whether changes in SCFA occur after trauma and hemorrhage in the feces and plasma of rodents. Materials and Methods: Polytrauma was induced in isoflurane-anesthetized Sprague-Dawley rats by damage to the small intestine, liver, right leg skeletal muscle, and femur, followed by 20% hemorrhage. Whole blood resuscitation was performed at 1 h (20%). Rats were euthanized at 2 h and feces and plasma were analyzed for short-chain fatty acids (SCFA) by liquid chromatography tandem mass spectroscopy. Results: Of 21 SCFA analyzed in the feces and plasma, 11 were measurable. In feces, five demonstrated a significant elevation after 2 h of severe trauma and hemorrhage (n-8) including propionic (37,775 ± 8,919 vs. 146,591 ± 46,734 nM/mg protein: mean ± SEM), pentanoic (10,975 ± 2,981 vs. 41,828 ± 10,645), 2-methyl propionic (2,621 ± 523 vs. 13,798 vs. 2083), 4-methyl pentanoic (1,134 ± 302 vs. 4,320 ± 1,029), and 3-phenyl propionic acid (42,194 ± 4,863 vs. 153,024 ± 38,473). The addition of whole blood resuscitation did not change these responses, but led to an additional significant elevation in butyric (68,551 ± 10,786 vs. 369,951 ± 79,515) and hexanoic acid (24,548 ± 6,791 vs. 102,002 ± 32,069). There was no change in SCFA after trauma, hemorrhage or resuscitation in the plasma (n = 6). Conclusion: Two hours of severe trauma and hemorrhage lead an elevation in many SCFAs in rat feces. No change in SCFA was found in plasma. Because SCFA are primarily derived from commensal bacteria in the gut, these data suggest that the measurement of SCFA could be used as an index of changes in the gut microbiome in pathological condition including trauma and hemorrhage.