Editing Neisseria gonorrhoeae (section)

=== Surface molecules ===
On its surface, ''N. gonorrhoeae'' bears hair-like [[Pilus|pili]], surface proteins with various functions, and sugars called [[Lipopolysaccharide|lipooligosaccharide]]. The pili mediate adherence, movement, and DNA exchange. The opacity-associated (Opa) proteins interact with the immune system, as do the [[Porin (protein)|porins]]. Lipooligosaccharide is an [[endotoxin]] that provokes an immune response. All of these are [[antigen]]ic and exhibit [[antigenic variation]]. The pili, Opa proteins, porins, and even the lipooligosaccharide have mechanisms to inhibit the immune response, making asymptomatic infection possible.<ref name="Edwards_2004">{{cite journal | vauthors = Edwards JL, Apicella MA | title = The molecular mechanisms used by Neisseria gonorrhoeae to initiate infection differ between men and women | journal = Clinical Microbiology Reviews | volume = 17 | issue = 4 | pages = 965–81, table of contents | date = October 2004 | pmid = 15489357 | pmc = 523569 | doi = 10.1128/CMR.17.4.965-981.2004 }}</ref>

==== Opa proteins ====
Phase-variable opacity-associated (Opa) adhesin proteins are used by ''N. gonorrhoeae'' as part of evading immune response in a host cell. At least 12 Opa proteins are known and the many variations of surface proteins make recognizing ''N. gonorrhoeae'' and mounting a defense by immune cells more difficult.<ref>{{cite web | title = STI Awareness: Gonorrhea | publisher = Planned Parenthood Advocates of Arizona | url = http://blog.advocatesaz.org/2011/04/11/sti-awareness-gonorrhea/ | archive-url = https://web.archive.org/web/20121103212554/http://blog.advocatesaz.org/2011/04/11/sti-awareness-gonorrhea/ | archive-date = 3 November 2012 | date = 11 April 2011 | access-date = 31 August 2011 }}</ref> Opa proteins are  in the outer membrane and facilitate a response when the bacteria interacts with a variety of host cells. These proteins bind to various epithelial cells, and allow ''N. gonorrhoeae'' to increase the length of infection as well as increase the amount of invasion into other host cells.<ref>{{cite journal | vauthors = Sadarangani M, Pollard AJ, Gray-Owen SD | title = Opa proteins and CEACAMs: pathways of immune engagement for pathogenic Neisseria | journal = FEMS Microbiology Reviews | volume = 35 | issue = 3 | pages = 498–514 | date = May 2011 | pmid = 21204865 | doi = 10.1111/j.1574-6976.2010.00260.x }}</ref>

==== Type IV pili ====
[[File:Type IV Pilus Twitching Motility Steps.svg|thumb|511x511px|''Neisseria gonorrhoeae'' use their type IV pili as a motility structure. These are the steps for the type IV pilus twitching motility mechanism.]]
Dynamic [[polymer]]ic protein filaments called [[Type IV pilus|type IV pili]] allow ''N. gonorrhoeae'' to do many bacterial processes including adhesion to surfaces, transformation competence, twitching motility, and immune response evasions.<ref name="Green_2022">{{cite book |doi=10.1016/bs.ampbs.2022.01.002 |title=Neisseria gonorrhoeae physiology and pathogenesis |series=Advances in Microbial Physiology |date=2022 |volume=80 |pages=35–83 |pmid=35489793 |isbn=978-0-323-98869-8 | vauthors = Green LR, Cole J, Parga EF, Shaw JG }}</ref> To enter the host the bacteria uses the pili to adhere to and penetrate mucosal surfaces. The pili are a pivotal [[virulence factor]] for ''N. gonorrhoeae''; without them, the bacterium is unable to promote colonization.<ref name="Hu_2020">{{cite journal | vauthors = Hu LI, Yin S, Ozer EA, Sewell L, Rehman S, Garnett JA, Seifert HS | title = Discovery of a New Neisseria gonorrhoeae Type IV Pilus Assembly Factor, TfpC | journal = mBio | volume = 11 | issue = 5 | date = October 2020 | pmid = 33109763 | doi = 10.1128/mBio.02528-20 | veditors = Justice S | pmc = 7593972 }}</ref> For motility, individual bacteria use their pili in a manner that resembles a grappling hook: first, they are extended from the cell surface and attach to a [[Substrate (biology)|substrate]]. Subsequent pilus retraction drags the cell forward. The resulting movement is referred to as twitching motility. ''N. gonorrhoeae'' is able to pull 100,000 times its own weight,<ref name="Merz_2000">{{cite journal | vauthors = Merz AJ, So M, Sheetz MP | title = Pilus retraction powers bacterial twitching motility | journal = Nature | volume = 407 | issue = 6800 | pages = 98–102 | date = September 2000 | pmid = 10993081 | doi = 10.1038/35024105 | bibcode = 2000Natur.407...98M }}</ref> and the pili used to do so are amongst the strongest biological motors known to date, exerting one [[Newton (unit)|nanonewton]].<ref name="Merz_2000" /> The PilF and PilT [[ATPase]] proteins are responsible for powering the extension and retraction of the type IV pilus, respectively. The adhesive functions of the gonococcal pilus play a role in [[microcolony]] aggregation and [[biofilm]] formation. These pili are also used to avoid immune responses from the cell they are invading by having their type IV pili antigenically vary. The main pilus filament is replaced by variable DNA sequences very frequently.<ref name="Green_2022" /> By doing this process rapidly, they are able to create a diversity of pili on their surface and evade the host cell's immune response.<ref name="Hu_2020" />

==== Lipooligosaccharide ====
Lipooligosaccharide is a low-weight version of lipopolysaccharide present on the surfaces of most other Gram-negative bacteria. It is a sugar (saccharide) side chain attached to lipid A (thus "lipo-") in the outer membrane coating the cell wall of the bacteria. The root "oligo" refers to the fact that it is a few sugars shorter than the typical lipopolysaccharide.<ref name="Sherris" /> As an endotoxin, it provokes inflammation. The shedding of lipooligosaccharide by the bacteria are sometimes responsible for issues associated with pelvic inflammatory disease.<ref name="Sherris" /> Although it functions primarily as an endotoxin, lipooligosaccharide may disguise itself with host [[sialic acid]] and block initiation of the [[Complement system|complement cascade]].<ref name="Sherris" />