4.3 - Protectins and bacterial infections
Bacterial infections have been found to influence PD1 levels. For
instance, infection with Borrelia sp. was shown to increase PD1
levels in the joints of mice (Blaho et al., 2009). Similarly, in a model
of antibiotic-induced dysbiosis in mice, Clostridium butyricum(C. butyricum ) infection led to elevated levels of PD1, resulting
in increased concentrations of IL-10, TGF-β1, and IL-4 produced by CD4+
T cells in the intestinal tract (Ariyoshi et al., 2021). These findings
suggest that PD1 plays an important endogenous role in these specific
contexts. Moreover, PD1 treatment has demonstrated positive effects on
bacterial infections. In vitro studies have shown that PD1 treatment
improves the uptake of E. coli by human macrophages and
neutrophils (Hamidzadeh et al., 2022; Chiang et al., 2012). In a mouse
model of peritonitis, activation of the G-protein coupled receptor 37
(GPR37) by PD1 during Listeria monocytogenes (L.
monocytogenes ) infection prevented mouse mortality, and PD1 treatment
resulted in decreased bacterial load in peritoneal fluids (Bang et al.,
2021). Although these studies are preliminary, they suggest a promising
role for PD1 and its potential therapeutic effects against bacterial
infections.