Inflammation and host-microbial interactions
Inflammation is elicited by the host in response to microbes and is believed to be essential for protection against infection. This process starts through the activation of innate immune cells expressing pattern recognition receptors (PRR) which recognize molecular patterns expressed by microorganisms (pathogen-associated molecular patternsĀ (PAMPs) or damage associated molecular pattern (DAMPs) released in response to them. An appropriate inflammatory response involves the coordinated production and release of molecules at the site of infection. This response restrains pathogen proliferation and is necessary for the ensuing adaptive immune response. In general, as the infection is controlled, the inflammatory response is followed by a resolution phase and return to homeostasis. However, excessive, or misplaced inflammation can be detrimental to the host, leading to further tissue damage and eventually death (Garcia et al, 2010; Sousa et al., 2020).
Many endogenous mediators have been described whose major function is to drive the resolution of inflammation. The various classes of mediators of resolution and major representatives in each class is given in Table 1. A review of the data that has led to their classification as pro-resolving molecules is beyond the scope of the current review but can be found at other recent reviews on the subject (see Sugimoto et al., 2019, Panigrahy et al, 2021, Feehan and Gilroy, 2019). As it will be discussed here, these so-called mediators of resolution tend to reduce inflammatory responses and to ameliorate the ability of the host to deal with bacterial and viral infections. As a corollary of the latter findings, we argue that the use of pro-resolving molecules or the activation of endogenous pro-resolving pathways during viral and bacterial infections may hold great promise as therapeutic strategies to avoid excessive inflammation without altering the ability of the host to deal infection.