Recent advances in understanding how the microbiome can influence both the physiology and the pathogenesis of disease in humans have highlighted the importance of gaining a deeper insight into the complexities of the host‐microbial dialogue. In tandem with this progress, has been a greater understanding of the biological pathways which regulate both homeostasis and inflammation at barrier tissue sites, such as the skin and the gut. In this regard, the Interleukin‐1 family of cytokines, which can be segregated into IL‐1, IL‐18 and IL‐36 subfamilies, have emerged as important custodians of barrier health and immunity. With established roles as orchestrators of various inflammatory diseases in both the skin and intestine, it is now becoming clear that IL‐1 family cytokine activity is not only directly influenced by external microbes, but can also play important roles in shaping the composition of the microbiome at barrier sites. This review explores the current knowledge surrounding the evidence that places these cytokines as key mediators at the interface between the microbiome and human health and disease at the skin and intestinal barrier tissues.

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Traumatic brain injury (TBI) is the most common cause of disability for millions of people worldwide. It is not only a health problem, but also an economic problem, as there is no effective treatment yet and the sequelae last for the rest of the patient’s life. After a TBI, acute phase proteins (APP) like serum amyloid A1 (SAA1) are released into the serum, promoting neuroinflammation among other things. It has been recently demonstrated that SAA1 binds to TLR4 and activates the production of proinflammatory cytokines, which in turn increases the production of SAA1. TAK242 administration, an antagonist of TLR4, shows protective effects in mice models after a TBI. Therefore, we hypothesize that using a molecule to neutralize SAA1 in serum will also reduce the neurological severity score (NSS) after inducing the closed head injury (CHI). The results showed that the intraperitoneal administration of this molecule can reduce the neurological damage in animals after TBI. Regarding the effects of this molecule at the inflammatory level, we have seen that the administration of this inhibitory compound of the SAA1 pathway produces a decrease in the gene expression of proinflammatory cytokines (IL-1β, IL6 and TNFα). This study demonstrates that SAA1 blockade can reduce neurological damage and the inflammatory genetic profile after trauma in an animal model.