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.