Table 1.
Pathogen-mediated modulation of mtROS.
| Pathogens | Study model | mtROS | Consequences | Mechanism of action | References |
|---|---|---|---|---|---|
| Bacteria | |||||
| A. baumannii | RAW264.7 cells | ↑ | Induction of pyroptosis and apoptosis | Activation of NLRP3 inflammasome | (38) |
| E. coli O157:H7 | Human colonic epithelial Caco-2 cells | ↑ | Induction of severe inflammation | Excessive ROS production from damaged mitochondria leading to NLRP3 inflammasome activation, which is inhibited by quercetin | (39) |
| P. aeruginosa | Primary murine neutrophils, HL-60 cells | ↑ | Neutrophil death | Pyocyanin-induced activation of neutrophil death through mitochondrial acid sphingomyelinase | (41) |
| P. gingivalis | Human primary gingival epithelial cells | ↓ | Increased bacterial survival and persistence | Inhibition of eATP/NOX2-ROS-antibacterial pathway | (44) |
| Human primary gingival epithelial cells | ↓ | Increased bacterial survival and persistence | Upregulation of the antioxidant glutathione responses to inhibit eATP-induced cytosolic and mtROS | (45) | |
| Parasite | |||||
| L. donovani | Murine peritoneal macrophages, in vivo | ↓ | Facilitation of parasite entry and survival | SREBP2-dependent upregulation of UCP2, a mitochondrial inner membrane protein, suppresses mtROS generation | (18) |
| RAW264.7 cells, murine splenic macrophages, in vivo | ↓ | Establishment of infection; anti-inflammatory immune responses | Upregulation of UCP2 suppresses mtROS; Inactivation of MAPK to ameliorate a Th1-biased immune responses | (19) | |
| T. cruzi | C2C12 cell line, human cardiac myocytes, HeLa, in vivo | ↑ | Heart failure in chagasic cardiomyopathy (CCM) | Excessive ROS-dependent inhibition in the nuclear translocation and activity of NFE2L2 (Nrf2) and induction of fibrotic gene expression | (46) |
| Virus | |||||
| RSV | A549 cells, vero cells, BCi-NS1 cells, pBECs | ↑ | Facilitation of viral infection | RSV induces mitochondrial redistribution, impairs mitochondrial respiration, loss of mitochondrial membrane potential | (47) |
| HIV | Human astrocytes | PI, ↓; NPI, ↑ | PI, astrocyte survival; NPI, Pyroptosis | PI, increased autophagic flux and activation of mitophagy; NPI, NLRP3-caspase-1-GSDMD pathway activation | (48) |
| IAV | In vivo; murine alveolar macrophages and neutrophils | ↑ | Exacerbation of viral pathogenesis | The mechanisms of IAV-mediated induction of mitoROS are not described; mitoTEMPO alleviates lung inflammation and attenuates the death of neutrophils and macrophages. | (49) |
| NHNE cells | ↑ | Restriction of IAV replication | Production of IFN-λ via mitochondrial and Duox2-grenerated ROS | (30) | |
| NHNE cells | ↑ | Inhibition of IAV viral titer | STAT phosphorylation and induction of IFN-stimulated genes | (31) | |
eATP, extracellular adenosine triphosphate; P2X7, purinergic receptor; NADPH, nicotinamide adenine dinucleotide phosphate; NOX2, NADPH oxidase 2; NLRP3, NLR family Pyrin domain-containing 3; SREBP2, sterol regulatory element binding protein 2; UCP2, uncoupling protein 2; MAPK, mitogen-activated protein kinase; NFE2L2 (Nrf2), nuclear factor erythroid 2-related factor 2; RSV, respiratory syncytial virus; pBEC, primary human bronchial epithelial cells; HIV, human immunodeficiency virus; PI, productively infected; NPI, nonproductively infected; GSDMD, gasdermin D; IAV, influenza A virus; NHNE, normal human nasal epithelial cells; IFN, interferon; Duox2, dual oxidase 2; STAT, signal transducer and activator of transcription; ↑, increase; ↓, decrease.