Editing Neisseria gonorrhoeae (section)

=== Iron ===
The general purpose of the ETC is the formation of the electrochemical gradient of hydrogen ions (H<sup>+</sup> or protons), resulting from concentration differences across the plasma membrane, needed to power ATP production in a process known as [[oxidative phosphorylation]].<ref name="Bacterial electron transport chains"/> In gonococci, movement of protons into the periplasmic space is accomplished by the Nuo complex I, the cytochrome ''bc<sub>1</sub>'' complex, and cytochrome ''ccb<sub>3</sub>''.<ref name="Green_2022" /><ref name="Aspholm_2010" /><ref name="Cytochrome bc1 complexes of microor"/> Subsequently, ATP synthesis is performed by the [[ATP synthase|F<sub>1</sub>F<sub>0</sub> ATP synthase]], a two-part protein complex present in gonococci as well as numerous other species across phylogenetic domains.<ref name="UniProt"/> This complex couples proton translocation back into the cytoplasm along its gradient with mechanical rotation to generate ATP.<ref name="Mechanism of the F1F0-type ATP"/>

To acquire the necessary iron, gonococci produce TonB-dependent transporters (TDTs) on the surface of their outer membrane that are able to directly extract iron, along with other metals, from their respective carrier proteins. Some of these include transferrin binding proteins A (TbpA) and B (TbpB), lactoferrin-binding proteins A (LbpA) and B (LbpB), and hemoglobin/hemoglobin-haptoglobin binding proteins HpuB and HpuA.<ref name="Green_2022" /><ref name="Stoudenmire_2022" /> In addition to these proteins, gonococci are also capable of using [[siderophore]]s, or compounds that are capable of chelating iron in the environment, that are produced by other bacteria; however, gonococcal cells are incapable of synthesizing siderophores themselves. These xenosiderophores are taken up by the TDT FetA through the outer membrane and then brought into the cell by the ''fetBCDEF'' transporter system.<ref name="Green_2022" /><ref name="Stoudenmire_2022">{{cite journal | vauthors = Stoudenmire JL, Greenawalt AN, Cornelissen CN | title = Stealthy microbes: How ''Neisseria gonorrhoeae'' hijacks bulwarked iron during infection | journal = Frontiers in Cellular and Infection Microbiology | volume = 12 | pages = 1017348 | date = 2022-09-15 | pmid = 36189345 | pmc = 9519893 | doi = 10.3389/fcimb.2022.1017348 | doi-access = free }}</ref>

Along with the sequestration defence that can be further upregulated by host inflammation, humans also produce [[siderocalin]]s that are able to chelate siderophores to as a further method of inhibiting pathogenic bacterial growth. These are sometimes ineffective against ''N. gonorrhoeae'', which is able to colonize intracellularly, particularly in phagocytic cells such as [[macrophage]]s and neutrophils. Increases in host intracellular iron also down regulates some of the intracellular pathogen-killing mechanisms; coincidentally, pathogenic ''Neisseria'' are able to alter several host cell mechanisms that ultimately allow the pathogen to take most of the available iron away from the host immune cell.<ref name="Stoudenmire_2022" />