LAUSR

Community-acquired pneumonia (CAP) is a worldwide prevalent infection and the most frequent cause of mortality due to infectious reasons [1]. Sepsis is present in one out of three hospitalized CAP patients already at diagnosis, and in some cases it appears within the first 48 h since onset of symptoms [2]. Sepsis, as defined in the New Consensus Sepsis (Sepsis-3), is considered a life-threatening organ dysfunction caused by a dysregulated host response against infection. In fact, it has been reported that, in CAP, the number of organ dysfunctions is the main mortality driver [3]. An adequate host response against infection requires an innate and adaptive immune response to locally get rid of microorganisms, avoiding its spread with deleterious systemic consequences. Neutrophils are rapidly recruited to lung after the innate response recognizes, through toll-like receptors (TLR), some patterns from microorganisms. TLRs are essential although they also contribute to tissue injury amplifying inflammation. Thus, that response needs to be well regulated because, as it has been found in previous studies, an excessive systemic inflammatory response may be detrimental for the host and increase treatment failure and mortality. In fact, initial elevated levels of interleukin (IL)-6, IL-8, and IL-10 depicted an inflammatory scenario that has been related to poor outcome [4]. Nevertheless, heterogeneous cytokine patterns have been reported across patients [5], related to the initial severity, the presence of comorbidities, and the causal microorganism [6]. All those studies bring to light how intricate the host response is.