The acute microbiota injury

Dear editor,

Hospital acquired infection (HAI) in intensive care unit (ICU) is a major public health issue associated with increased morbi-mortality and costs. Over the years our perception and our understanding of the pathophysiology of HAI as evolved but the treatment remains basically limited to antimicrobial therapy [1]. In critically ill patients, there is evidence that the alteration of the interaction between the immune system and the microbiota could promotes the occurrence of HAI [1]. Accordingly, limiting microbiota injuries during the ICU stays could be a major mean to prevent HAI.

Nowadays, it is well established that all the epithelia are colonized by a diverse and dynamic living ecosystem composed of microorganisms, viruses and fungi. The microbiota, referring to the different communities of bacteria living symbiotically with our epithelia, participate to the proper development and functioning of our metabolic pathways (i.e. cognitive and immunity development) through a constant crosstalk between host and bacteria [2]. These microbiotas are constitutive of the human being [3,4,5]. We are not only a multicellular eukaryotes organism but a holobiont, an assemblage of different species of organisms, a Homo microbicus. [2, 6]

Healthy microbiota promotes host defense effectors, plays the role of a physical and functional barriers and inhibits the growth of pathogenic bacteria [7]. Conversely, altered microbiota (i.e. dysbiosis) plays an important role on the pathophysiology of immune and inflammatory disease: skin microbiotal dysbiosis is associated with the onset of atopic dermatitis, alteration of lung microbiota may be associated with asthma development and/or hospital-acquired pneumonia and gut microbiota dysbiosis plays a predominant role in Crohn’s disease [1, 8] Immunity and microbiota are interdependent, thus the alteration of one could lead to the alteration of the other [9].

Critically ill patients are exposed to conditions that impaired one or more physiologic functions commonly referred as acute injury (i.e. acute lung injury, acute kidneys injury). These injuries could result of either the direct hit of the organ or the consequences of an acute systemic response leading to potential complications and worsened outcomes.

As for other organs, the function of microbiota could be impaired in case of acute injury and strained its resilience. In critically ills patients, several factors, some intrinsic, some related to the underlying disease or iatrogenic, may promote dysbiosis (decrease in bacterial diversity, loss of commensal bacteria and increase of pathogenic bacterial inoculum) [1]. Accordingly, the alteration of lung microbiota is associated with the development of hospital-acquired pneumonia and acute respiratory syndrome [1]. Likewise, gut microbiota dysbiosis promotes colitis and play a role in acute kidneys injury [10].

These considerations lead us to propose the term of acute microbiota injury (AMI) for the critically ill, which could be approached as followed: acute microbiota injury correspond to the quantitative and/or qualitative alteration of patient microbiota leading to potential dysbiosis. It could selectively affect a particular microbiota (i.e. lung microbiota in case of mechanical ventilation) or all of them simultaneously. Factors promoting microbiota injury are numerous and related to the severity of the underlying disease, the alteration of the immunity, the patient medical history, the use of mechanical ventilation and various other treatments such as antibiotics, steroids or sedation drugs [1]. We believe that the concept of AMI should be incorporated in our thinking at the bedside. Because there is a close relationship between immunity and microbiota, the potential harmful effect of a therapeutic on microbiota should be assessed when introducing it.

Microbiota, the forgotten organ, and its acute injury among patient hospitalized in ICU is now established. The conceptual legacy of Koch and Pasteur has delayed our awareness on its importance. A better understanding of its quantitative and qualitative changes as well as of the factors influencing it over time is mandatory. For the future, we should look toward the development of specific tools allowing clinician to assess and follow global and specific microbiota injury over time. In the meantime, preventive means (i.e. avoiding inappropriate administration of antimicrobial therapy) are our best ally to limit the severity of acute microbiota injuries.