|
| Bacteria | Gram stain | Induction of type I IFN | Role of type I IFN | Effects on host | References |
|
| C. trachomatis/muridarum | − | cGAS generates cGAMP from Chlamydial
DNA which activates STING/IRF3 | (1) Beneficial | (1) Depletes intracellular iron and regulates
IDO which can alter tryptophan availability
to bacteria; IFN-α together with IFN-γ or
TNF-α has synergistic antichlamydial effect | [44, 71–73] |
| (2) Detrimental | (2) Decreased chlamydia-specific T cells and
decreased CXCL9-induced T cell
recruitment prevent bacterial clearance |
|
| L. monocytogenes | + | DNA- or CDN-mediated signaling via
IFI16 and STING, RNA signaling via RIG-I
or MDA5, RNA Pol III transcription of DNA
to RNA, NOD2 detection of MDP in
conjunction with cytosolic detection of DNA | (1) Beneficial | (1) Decreases inflammatory pathology in
liver and induces rapid protective cytokine
response after intragastric infection | [43, 49, 74, 79–84,
87–89, 91–93, 95] |
| (2) Detrimental | (2) Increases expression of apoptotic genes
and increases apoptosis of lymphocytes and
macrophages needed for bacterial clearance,
decreases production of antibacterial
IL-12p70, and decreases TNF-α secretion
from macrophages; dampened macrophage
responsiveness to IFN-γ makes these cells
more permissive to infection/replication,
decreases numbers of IL-17A-secreting
γδ T cells thereby decreasing neutrophil
recruitment and bacterial control in the
spleen, increases cell-to-cell spread of
bacteria, and inhibits CD8 T cell priming |
|
| M. tuberculosis | NA | cGAS-dependent generation of CDNs
which activate STING, NOD2 detects
Mycobacterial MDP leading to activation
of RIP2 and IRF5 | (1) Beneficial | (1) Hypervirulent strain promotes alternative
macrophage activation in the absence
of IFN-γ that controls bacterial replication | [20, 41, 42, 98, 105–107] |
| (2) Detrimental | (2) Dampens antibacterial IL-1β production,
IL-10 downstream of type I IFNs reduces
antibacterial activity of IFN-γ; causes
fatal inflammation due to increased
chemokine production, neutrophil
recruitment to the lung, and alveolar
macrophage death |
|
S. enterica serovar
Typimurium | − | TRIF-dependent TLR3 and TLR4 signaling
likely via nucleic acids and LPS, respectively,
RIG-I detection of RNA | (1) Beneficial | (1) Important for antibacterial macrophage
responses | [111–114, 118,
120–122, 124] |
| (2) Detrimental | (2) Increased caspase-11-mediated
macrophage death allowing bacterial
release which is exacerbated in the
absence of caspase-1, a protein required
for neutrophilic control of infection, increases
RIP1/RIP3-mediated macrophage death;
suppresses IL-1 cytokine and neutrophil
chemoattractant transcripts in macrophages
which decreases bacterial control;
influenza-induced type I IFNs negatively
impact gut microbiota and decrease innate
responses in the gut, increasing
susceptibility to S. enterica |
|
| F. tularensis | − | cGAS, IFI204, STING, and IRF3-dependent | (1) Beneficial | (1) Type I IFN-induced GBPs activate AIM2
inflammasome leading to macrophage
pyroptosis and removal of
replicative niche | [91, 126, 135–139] |
| (2) Detrimental | (2) Decreased number of IL-17A-secreting
γδ T cells which are important for
neutrophil recruitment to the spleen
and bacterial control |
|
| B. abortus | − | RNA Pol III and/or STING are
required for type I IFN induction in a
MyD88-dependent but TRIF-
and TLR-independent manner | (1) Detrimental | (1) Alters DC maturation which dampens
DC cytokine production; increases bacterial
load due to decreases in IFN-γ and NO
production; increases splenocyte
apoptosis and Trail expression in
macrophages | [36, 141, 144] |
|
| L. pneumophila | − | RIG-I detection of RNA and subsequent
signaling through IPS-1 and IRF3, RNA
Pol III-dependent transcription of DNA to
RNA then signaling via RIG-I and IPS-1,
CDN detection via STING | (1) Beneficial | (1) Controls bacterial replication within host
cell vacuoles; promotes inflammatory
macrophage polarization and
bacterial clearance | [47, 82, 150–154] |
|
| C. burnetii | − | NOD1/2, RIG-I, and/or TLR7/9-mediated
production of IFN- α in pDCs, involves IRF7 | (1) Beneficial | (1) Administration to lung was
protective—mechanism unknown at
this time | [167, 169] |
| (2) Detrimental | (2) Lack of IFNAR benefited host; i.p.
delivery of IFN-α was harmful to host
perhaps due to suppression of necessary
inflammatory cytokines |
|
