Editing Reactive oxygen species (section)

===Pathogen response===
When a plant recognizes an attacking pathogen, one of the first induced reactions is to rapidly produce [[superoxide]] ({{chem|O|2|-}}) or [[hydrogen peroxide]] ({{chem|H|2|O|2}}) to strengthen the cell wall. This prevents the spread of the pathogen to other parts of the plant, essentially forming a net around the pathogen to restrict movement and reproduction.

In the mammalian host, ROS is induced as an antimicrobial defense.<ref name="Functions of ROS in Macrophages and" /> To highlight the importance of this defense, individuals with [[chronic granulomatous disease]] who have deficiencies in generating ROS, are highly susceptible to infection by a broad range of microbes including ''[[Salmonella enterica]]'', ''[[Staphylococcus aureus]]'', ''[[Serratia marcescens]]'', and ''[[Aspergillus]]'' spp.

Studies on the [[homeostasis]] of the ''[[Drosophila melanogaster]]'''s intestines have shown the production of ROS as a key component of the immune response in the gut of the fly. ROS acts both as a bactericide, damaging the bacterial DNA, RNA and proteins, as well as a signalling molecule that induces repair mechanisms of the [[epithelium]].<ref>{{Cite journal |vauthors=Buchon N, Broderick NA, Lemaitre B |date=September 2013 |title=Gut homeostasis in a microbial world: insights from Drosophila melanogaster |url=http://infoscience.epfl.ch/record/189299 |journal=Nature Reviews. Microbiology |volume=11 |issue=9 |pages=615–626 |doi=10.1038/nrmicro3074 |pmid=23893105 |s2cid=8129204}}</ref> The [[uracil]] released by microorganism triggers the production and activity of DUOX, the ROS-producing enzyme in the intestine. DUOX activity is induced according to the level of uracil in the gut; under basal conditions, it is down-regulated by the protein kinase [[Mitogen-activated protein kinase|MkP3]]. The tight regulation of DUOX avoids excessive production of ROS and facilitates differentiation between benign and damage-inducing microorganisms in the gut.<ref>{{Cite journal |display-authors=6 |vauthors=Lee KA, Kim SH, Kim EK, Ha EM, You H, Kim B, Kim MJ, Kwon Y, Ryu JH, Lee WJ |date=May 2013 |title=Bacterial-derived uracil as a modulator of mucosal immunity and gut-microbe homeostasis in Drosophila |journal=Cell |volume=153 |issue=4 |pages=797–811 |doi=10.1016/j.cell.2013.04.009 |pmid=23663779 |doi-access=free}}</ref>

The manner in which ROS defends the host from invading microbe is not fully understood. One of the more likely modes of defense is damage to microbial DNA. Studies using ''Salmonella'' demonstrated that DNA repair mechanisms were required to resist killing by ROS. A role for ROS in antiviral defense mechanisms has been demonstrated via Rig-like helicase-1 and mitochondrial antiviral signaling protein. Increased levels of ROS potentiate signaling through this mitochondria-associated antiviral receptor to activate interferon regulatory factor (IRF)-3, IRF-7, and nuclear factor kappa B (NF-κB), resulting in an antiviral state.<ref name="pmid21597473">{{Cite journal |vauthors=West AP, Shadel GS, Ghosh S |date=June 2011 |title=Mitochondria in innate immune responses |journal=Nature Reviews. Immunology |volume=11 |issue=6 |pages=389–402 |doi=10.1038/nri2975 |pmc=4281487 |pmid=21597473}}</ref> Respiratory epithelial cells induce mitochondrial ROS in response to influenza infection. This induction of ROS led to the induction of type III interferon and the induction of an antiviral state, limiting viral replication.<ref name="pmid23786562">{{Cite journal |display-authors=6 |vauthors=Kim HJ, Kim CH, Ryu JH, Kim MJ, Park CY, Lee JM, Holtzman MJ, Yoon JH |date=November 2013 |title=Reactive oxygen species induce antiviral innate immune response through IFN-λ regulation in human nasal epithelial cells |journal=American Journal of Respiratory Cell and Molecular Biology |volume=49 |issue=5 |pages=855–865 |doi=10.1165/rcmb.2013-0003OC |pmc=5455605 |pmid=23786562}}</ref> In host defense against mycobacteria, ROS play a role, although direct killing is likely not the key mechanism; rather, ROS likely affect ROS-dependent signalling controls, such as cytokine production, autophagy, and granuloma formation.<ref>{{Cite journal |display-authors=6 |vauthors=Herb M, Gluschko A, Wiegmann K, Farid A, Wolf A, Utermöhlen O, Krut O, Krönke M, Schramm M |date=February 2019 |title=Mitochondrial reactive oxygen species enable proinflammatory signaling through disulfide linkage of NEMO |journal=Science Signaling |volume=12 |issue=568 |pages=eaar5926 |doi=10.1126/scisignal.aar5926 |pmid=30755476 |doi-access=free}}</ref><ref>{{Cite journal |vauthors=Deffert C, Cachat J, Krause KH |date=August 2014 |title=Phagocyte NADPH oxidase, chronic granulomatous disease and mycobacterial infections |journal=Cellular Microbiology |volume=16 |issue=8 |pages=1168–1178 |doi=10.1111/cmi.12322 |pmid=24916152 |s2cid=3489742 |doi-access=free}}</ref>

Reactive oxygen species are also implicated in activation, [[Clonal anergy|anergy]] and apoptosis of [[T cells]].<ref>{{Cite journal |vauthors=Belikov AV, Schraven B, Simeoni L |date=October 2015 |title=T cells and reactive oxygen species |journal=Journal of Biomedical Science |volume=22 |pages=85 |doi=10.1186/s12929-015-0194-3 |pmc=4608155 |pmid=26471060 |doi-access=free}}</ref>