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陰道菌群:修订间差异

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[[File:Glycogen structure.svg |thumb|100px|糖原是存在在[[陰道上皮]]中的糖,會分解成乳酸]]
[[File:Glycogen structure.svg |thumb|100px|糖原是存在在[[陰道上皮]]中的糖,會分解成乳酸]]
一般認為低pH值是控制陰道菌群生成的主要機制。雖然乳桿菌產生的乳酸會讓陰道變酸性,不過尚未證明其為陰道酸性的主要來源,目前只確定的是大部份的乳桿菌在pH < 4.5時可以生長的最好<ref name=" Aroutcheva ">{{cite journal |author1=Aroutcheva A. |author2=Gariti D. |author3=Simon M. |author4=Shott S. |author5=Faro J. |author6=Simoes J. A. |author7=Gurguis A. |author8=Faro S. | year = 2001 | title = Defense factors of vaginal lactobacilli | url = | journal = Am. J. Obstet. Gynecol. | volume = 185 | issue = | pages = 375–379 }}</ref><ref>{{cite journal | author = Linhares I. M., Summers P. R., Larsen B., Giraldo P. C., Witkin S. S. | year = 2011 | title = Contemporary perspectives on vaginal pH and lactobacilli | url = | journal = Am. J. Obstet. Gynecol. | volume = 204 | issue = | page = 120.e1–120.e5 | doi=10.1016/j.ajog.2010.07.010}}</ref><ref>{{cite journal |author1=Redondo-Lopez V. |author2=Cook R. L. |author3=Sobel J. D. | year = 1990 | title = Emerging role of lactobacilli in the control and maintenance of the vaginal bacterial microflora | url = | journal = Rev. Infect. Dis. | volume = 12 | issue = | pages = 856–872 | doi=10.1093/clinids/12.5.856}}</ref>。
一般認為低pH值是控制陰道菌群生成的主要機制。雖然乳桿菌產生的乳酸會讓陰道變酸性,不過尚未證明其為陰道酸性的主要來源,目前只確定的是大部份的乳桿菌在pH < 4.5時可以生長的最好<ref name=" Aroutcheva ">{{cite journal |author1=Aroutcheva A. |author2=Gariti D. |author3=Simon M. |author4=Shott S. |author5=Faro J. |author6=Simoes J. A. |author7=Gurguis A. |author8=Faro S. | year = 2001 | title = Defense factors of vaginal lactobacilli | url = | journal = Am. J. Obstet. Gynecol. | volume = 185 | issue = | pages = 375–379 }}</ref><ref>{{cite journal | author = Linhares I. M., Summers P. R., Larsen B., Giraldo P. C., Witkin S. S. | year = 2011 | title = Contemporary perspectives on vaginal pH and lactobacilli | url = | journal = Am. J. Obstet. Gynecol. | volume = 204 | issue = | page = 120.e1–120.e5 | doi=10.1016/j.ajog.2010.07.010}}</ref><ref>{{cite journal |author1=Redondo-Lopez V. |author2=Cook R. L. |author3=Sobel J. D. | year = 1990 | title = Emerging role of lactobacilli in the control and maintenance of the vaginal bacterial microflora | url = | journal = Rev. Infect. Dis. | volume = 12 | issue = | pages = 856–872 | doi=10.1093/clinids/12.5.856}}</ref>。

=== 過氧化氫 ===
產生過氧化氫(H<SUB>2</SUB>O<SUB>2</SUB>)是眾所週知的抗菌機制<ref>{{cite journal |author1=Dahiya R. S. |author2=Speck M. L. | year = 1968 | title = Hydrogen peroxide formation by lactobacilli and its effect on ''Staphylococcus aureus'' | url = | journal = J. Dairy Sci. | volume = 51 | issue = | pages = 1568–1572 | doi=10.3168/jds.s0022-0302(68)87232-7}}</ref><ref>{{cite journal |author1=Thompson R. |author2=Johnson A. | year = 1951 | title = The inhibitory action of saliva on the diphtheria Bacillus: Hydrogen peroxide, the inhibitory agent produced by salivary streptococci | url = | journal = J. Infect. Dis. | volume = 88 | issue = | pages = 81–85 | doi=10.1093/infdis/88.1.81}}</ref><ref>{{cite journal |author1=Wheater D. M. |author2=Hirsch A. |author3=Mattick A. T. R. | year = 1952 | title = Possible identity of lactobacillin with hydrogen peroxide produced by lactobacilli | url = | journal = Nature | volume = 170 | issue = | pages = 623–624 | doi=10.1038/170623a0}}</ref>,透過直接作用或是透過人類的骨髓過氧化酶抑制微生物成長<ref name=" Eschenbach1 ">{{cite journal |author1=Eschenbach D. A. |author2=Davick P. R. |author3=Williams B. L. |author4=Klebanoff S. J. |author5=Young-Smith K. |author6=Critchlow C. M. |author7=Holmes K. K. | year = 1989 | title = Prevalence of hydrogen peroxide-producing ''Lactobacillus'' species in normal women and women with bacterial vaginosis | url = | journal = J. Clin. Microbiol. | volume = 27 | issue = | pages = 251–256 }}</ref><ref name=" Hillier1 ">{{cite journal |author1=Hillier S. L. |author2=Krohn M. A. |author3=Klebanoff S. J. |author4=Eschenbach D. A. | year = 1992 | title = The relationship of hydrogen peroxide-producing lactobacilli to bacterial vaginosis and genital microflora in pregnant women | url = | journal = Obstet. Gynecol. | volume = 79 | issue = | pages = 369–373 | doi=10.1097/00006250-199203000-00008}}</ref><ref name=" Klebanoff 1 ">{{cite journal | author = Klebanoff SJ | year = 1970 | title = Peroxidase-mediated antimicrobial activity of rat uterine fluid | url = | journal = Gynecol Invest | volume = 1 | issue = | pages = 21–30 | doi=10.1159/000301903}}</ref>。會產生過氧化氫的乳桿菌可以使HIV-1、單純皰疹病毒第2型(HSV-2)、陰道毛滴蟲、陰道加德諾菌、''P. bivia''及大腸桿菌去活化。O'Hanlon<ref name="O'Hanlon1" />和Baeten<ref>{{cite journal |author1=Baeten J. M. |author2=Hassan W. M. |author3=Chohan V. |author4=Richardson B. A. |author5=Mandaliya K. |author6=Ndinya-Achola J. O. |author7=Jaoko W. |author8=McClelland R. S. | year = 2009 | title = Prospective study of correlates of vaginal Lactobacillus colonisation among high-risk HIV-1 seronegative women | url = | journal = Sex. Transm. Infect. | volume = 85 | issue = | pages = 348–353 | doi=10.1136/sti.2008.035451|pmc=2837477 }}</ref>發現在健康女性的陰道生態系中,有96%的乳桿菌屬細菌會產生H<SUB>2</SUB>O<SUB>2</SUB>(其中以''L. jensenii''和''L. vaginalis''生成的比例最高)<ref name="Martin1" /><ref>{{cite journal | author = Wilks M., Wiggins R., Whiley A., Hennessy E., Warwick S., Porter H., Corfield A., Millar M. | year = 2004 | title = Identification and H<SUB>2</SUB>O<SUB>2</SUB> production of vaginal lactobacilli from pregnant women at high risk of preterm birth and relation with outcome | url = | journal = J. Clin. Microbiol. | volume = 42 | issue = | pages = 713–717 | doi=10.1128/jcm.42.2.713-717.2004| pmc = 344438}}</ref>,若是有陰道細菌炎的女性,其陰道生態系中只有6%的乳桿菌屬細菌會產生H<SUB>2</SUB>O<SUB>2</SUB><ref name=" Eschenbach1 " />。{{transh}}In agreement with this, ''L. iners'', most frequently associated with disturbed vaginal microflora,<ref name=" Verhelst1 ">{{cite journal | author = Verhelst R., Verstraelen H., Claeys G., Verschraegen G., Simaey L. Van, De Ganck C., De Backer E., Temmerman M., Vaneechoutte M. | year = 2005 | title = Comparison between Gram stain and culture for the characterization of vaginal microflora: Definition of a distinct grade that resembles grade I microflora and revised categorization of grade I microflora | url = | journal = BMC Microbiol. | volume = 5 | issue = | page = 61 }}</ref><ref name=" De Backer1 ">{{cite journal | author = De Backer E., Verhelst R., Verstraelen H., Alqumber M. A., Burton J. P., Tagg J. R., Temmerman M., Vaneechoutte M. | year = 2007 | title = Quantitative determination by real-time PCR of four vaginal ''Lactobacillus'' species, ''Gardnerella vaginalis'' and ''Atopobium vaginae'' indicates an inverse relationship between ''L. gasseri'' and ''L. iners'' | url = | journal = BMC Microbiol. | volume = 7 | issue = | page = 115 | doi=10.1186/1471-2180-7-115}}</ref> is a poor producer of H<SUB>2</SUB>O<SUB>2</SUB>.<ref name=" Antonio1 ">{{cite journal |author1=Antonio M. A. |author2=Hawes S. E. |author3=Hillier S. L. | year = 1999 | title = The identification of vaginal ''Lactobacillus'' species and the demographic and microbiologic characteristics of women colonized by these species | url = | journal = J. Infect. Dis. | volume = 180 | issue = | pages = 1950–1956 | doi=10.1086/315109 | pmid=10558952}}</ref><ref>{{cite journal |author1=Antonio M. A. D. |author2=Rabe L. K. |author3=Hillier S. L. | year = 2005 | title = Colonization of the rectum by Lactobacillus species and decreased risk of bacterial vaginosis | url = | journal = J. Infect. Dis. | volume = 192 | issue = | pages = 394–398 | doi=10.1086/430926}}</ref> Vaginal colonization by H<SUB>2</SUB>O<SUB>2</SUB>-producing lactobacilli has been associated with a decrease in the occurrence of <!-- [[bacterial vaginosis]] -->[[细菌性阴道病]] (BV).<ref>{{cite journal |author1=Hawes S. E. |author2=Hillier S. L. |author3=Benedetti J. |author4=Stevens C. E. |author5=Koutsky L. A. |author6=Wolner-Hanssen P. L. |author7=Holmes K. K. | year = 1996 | title = Hydrogen peroxide-producing lactobacilli and acquisition of vaginal infections | url = | journal = J. Infect. Dis. | volume = 174 | issue = | pages = 1058–1063 | doi=10.1093/infdis/174.5.1058}}</ref> However, more recently O'Hanlon et al.<ref name=" O'Hanlon2 ">{{cite journal | author = O'Hanlon D. E., Lanier B. R., Moench T. R., Cone R. A. | year = 2010 | title = Cervicovaginal fluid and semen block the microbicidal activity of hydrogen peroxide produced by vaginal lactobacilli | url = | journal = BMC Infect. Dis. | volume = 10 | issue = | page = 120 | doi=10.1186/1471-2334-10-120}}</ref> demonstrated that cervicovaginal fluid and semen have a significant H<SUB>2</SUB>O<SUB>2</SUB>-blocking activity and they later <ref name=" O'Hanlon1 " /> demonstrated that physiological concentrations of H<SUB>2</SUB>O<SUB>2</SUB> below 100 μM
fail to inactivate any of the 17 tested BV-associated bacteria, e.g. ''A. vaginae'', ''G. vaginalis'', ''Mobiluncus'' spp., ''P. bivia'', ''Prevotella corporis'', ''Mycoplasma hominis'', even in the presence of
human myeloperoxidase, known to increase the microbicidal activity of H<SUB>2</SUB>O<SUB>2</SUB>.<ref name=" O'Hanlon1 " /> Only supraphysiologic concentrations of exogenous H<SUB>2</SUB>O<SUB>2</SUB> (0.34% w/v, 100 mM) were sufficient to inactivate BV-associated bacteria at which concentration it more potently inactivated vaginal lactobacilli (''L. crispatus'', ''L. gasseri'', ''L. iners'' and ''L. jensenii''). A concentration of 100 mM H<SUB>2</SUB>O<SUB>2</SUB> is approximately 50-fold higher than lactobacilli are capable of producing even under optimal aerobic, low-antioxidant conditions, and approximately 5,000-fold higher than the estimated H<SUB>2</SUB>O<SUB>2</SUB> concentration in vivo. Even more remarkable, the addition of only 1% vaginal fluid blocked the microbicidal activity of 1 M H<SUB>2</SUB>O<SUB>2</SUB>. Possible explanations may be that cervicovaginal fluid and semen contain proteins, glycoproteins, polysaccharides, lipids, and other molecules with the potential to react with and inactivate H<SUB>2</SUB>O<SUB>2</SUB>. In addition, the vagina is hypoxic most of the time, whereas lactobacilli require oxygen to produce hydrogen peroxide. It is also remarkable that catalase, which provides bacteria protection against toxic H<SUB>2</SUB>O<SUB>2</SUB>, is absent in lactobacilli,<ref name=" Eschenbach1 " /><ref name=" Klebanoff ">{{cite journal |author1=Klebanoff S. J. |author2=Hillier S. L. |author3=Eschenbach D. A. |author4=Waltersdorph A. M. | year = 1991 | title = Control of the microbial flora of the vagina by H202-generating lactobacilli | url = | journal = J. Infect. Dis. | volume = 164 | issue = | pages = 94–100 | doi=10.1093/infdis/164.1.94}}</ref> and as such they would be unprotected against their own H<SUB>2</SUB>O<SUB>2</SUB> production. In contrast, under optimal anaerobic growth conditions, physiological concentrations of lactic acid inactivated the BV-associated pathogens without affecting the vaginal lactobacilli.<ref name=" O'Hanlon1 " /><ref name=" O'Hanlon2 " /> In summary, although the hydrogen peroxide production of lactobacilli has been considered as an important antimicrobial component, contributing to the colonization resistance provided by lactobacilli,<ref name=" Martin1 " /><ref name=" Vallor ">{{cite journal |author1=Vallor A. C. |author2=Antonio M. A. |author3=Hawes S. E. |author4=Hillier S. L. | year = 2001 | title = Factors associated with acquisition of, or persistent colonization by, vaginal lactobacilli: Role of hydrogen peroxide production | url = | journal = J. Infect. Dis. | volume = 184 | issue = | pages = 1431–1436 | doi=10.1086/324445}}</ref> and although there seems to be a link between H<SUB>2</SUB>O<SUB>2</SUB>-producing lactobacilli and normal vaginal microflora, recent data do not support this role for H<SUB>2</SUB>O<SUB>2</SUB>.<ref name=" O'Hanlon1 " /><ref name=" O'Hanlon2 " />
{{transf}}


==其他菌群==
==其他菌群==

2018年12月18日 (二) 16:54的版本

乳桿菌以及陰道的上皮組織細胞

陰道菌群(Vaginal flora)或陰道微生物(vaginal microbiota)是在阴道內生長的微生物,是由德國婦科醫生艾伯特·竇特蘭英语Albert Döderlein在1892年發現[1],是人類微生物群系中的一部份。細菌的數量和種類可以反映女性的身體健康情形。健康女性陰道內主要的細菌是乳桿菌屬[2](例如卷曲乳杆菌英语Lactobacillus crispatus),普遍認為這種細菌分泌的乳酸可以避免致病原的感染[3]

乳桿菌

健康女性陰道內主要的細菌是乳桿菌屬的細菌[2],自從竇特蘭首次提到陰道中的乳桿菌起,一般都認為乳桿菌有助於維持陰道內的生態系統。已證實乳桿菌可以抑制致病微生物的生長,例如梭樣類桿菌英语Bacteroides fragilis大腸桿菌陰道加德諾菌英语Gardnerella vaginali、动弯杆菌属、淋球菌Peptostreptococcus anaerobiusP. bivia金黃色葡萄球菌等。一般認為抑制致病微生物的作用是透過乳酸進行的[4][5][6][7]。而且乳桿菌屬會附著在陰道上皮細胞,因此可以避免其他致病菌的感染以及長期生長[8]

乳桿菌可以製造乳酸,並且乳桿菌會附著在陰道上皮組織,影響其他微生物的生長,其他陰道內的拮抗作用包括產生过氧化氢(廣譜抗菌劑)以及細菌素英语bacteriocin(靶特異性抗菌劑)[9][10]

產生乳酸

糖原是存在在陰道上皮中的糖,會分解成乳酸

一般認為低pH值是控制陰道菌群生成的主要機制。雖然乳桿菌產生的乳酸會讓陰道變酸性,不過尚未證明其為陰道酸性的主要來源,目前只確定的是大部份的乳桿菌在pH < 4.5時可以生長的最好[11][12][13]

過氧化氫

產生過氧化氫(H2O2)是眾所週知的抗菌機制[14][15][16],透過直接作用或是透過人類的骨髓過氧化酶抑制微生物成長[17][18][19]。會產生過氧化氫的乳桿菌可以使HIV-1、單純皰疹病毒第2型(HSV-2)、陰道毛滴蟲、陰道加德諾菌、P. bivia及大腸桿菌去活化。O'Hanlon[10]和Baeten[20]發現在健康女性的陰道生態系中,有96%的乳桿菌屬細菌會產生H2O2(其中以L. jenseniiL. vaginalis生成的比例最高)[9][21],若是有陰道細菌炎的女性,其陰道生態系中只有6%的乳桿菌屬細菌會產生H2O2[17]

其他菌群

一般女性的陰道菌群是以乳桿菌為主,不過可能會隨種族而有些差異。有些女性的陰道菌群中,有一部份是非致病英语Nonpathogenic organisms微生物[22][30],不少研究指出,在健康無症狀的女性(特別是黑人及西班裔女性)中,有不少人(佔7~33%)[31]的陰道菌群中乳桿菌的含量不多[32][33],而其菌群主要是由其他會分泌乳酸的細菌組成,例如阿托波菌、纖毛菌、明串珠菌、巨球型菌、片球菌、鏈球菌及魏斯氏菌[34][32][31],所有的女性陰道菌群中都有會分泌乳酸的細菌[32][31]。不是所有的菌群都有相同的韌性,因此若陰道菌群韌性較低,其菌群結構可能會因為一些外在擾動(例如月經、性交、陰道沖洗或是避孕措施)而變化。這些陰道菌群結構及組成的差異也可能是造成一些女性較容易罹患細菌性陰道炎及其他陰道感染的原因[31][35][36]。陰道菌群可能會被外在因素影響,而其他菌種也會分泌乳酸[37],陰道的pH值以及產生酸的環境會形成正常的陰道菌群,在懷孕時,其pH值會進一步降低[38]

其他陰道中的細菌

其他陰道中常見的微生物,革蘭氏陽性的球菌有陰道阿托波氏菌、消化鏈球菌、葡萄球菌屬、鏈球菌屬、和擬桿菌屬、梭狀芽孢桿菌屬、陰道加德納菌屬、Mobiluncus及普氏菌屬,也有革蘭氏陰性腸道生物,例如大腸桿菌[22][23]。陰道中也常會發現支原體和解脲支原體。其中一些專性和兼性厭氧細菌和細菌性陰道炎有關[33]

懷孕

使用衛生棉條對陰道菌群的影響目前仍有爭議,不過適當的使用衛生棉條不會大幅改變陰道菌群的平衡[需要可靠醫學來源]。懷孕會改變陰道菌群,也會減少菌種的多樣性[39]

疾病預防

健康的陰道菌群可以維持酸性環境(< 4.5),預防细菌性阴道病、念珠菌症等疾病,這種酸性環境不利於常見的致病原,像是陰道加德諾菌。在健康陰道菌群中,乳桿菌也佔據了生態位,不然會被其他的致病原所佔據[需要可靠醫學來源]

细菌性阴道病和陰道中出現陰道加德諾菌英语Gardnerella vaginalis消化鏈球菌英语Peptostreptococcus anaerobius有關[40],也和構成健康陰道微生物群的乳桿菌種類減少有關[39][41][42][43]

研究

目前研究發現陰道存在乳酸桿菌為主的菌群,和性傳染疾病發生率較低有關[44][45]

相關條目

參考資料

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  2. ^ 2.0 2.1 Vasquez, A.; Jakobsson, T.; Ahrne, S.; Forsum, U.; Molin, G. Vaginal Lactobacillus Flora of Healthy Swedish Women. Journal of Clinical Microbiology. 2002, 40 (8): 2746–2749. PMC 120688可免费查阅. PMID 12149323. doi:10.1128/JCM.40.8.2746-2749.2002. 
  3. ^ Witkin, S. S.; Linhares, I. M.; Giraldo, P. Bacterial flora of the female genital tract: Function and immune regulation. Best Practice & Research Clinical Obstetrics & Gynaecology. 2007, 21 (3): 347–354. PMID 17215167. doi:10.1016/j.bpobgyn.2006.12.004. 
  4. ^ Graver M., Wade J. The role of acidification in the inhibition of Neisseria gonorrhoeae by vaginal lactobacilli during anaerobic growth. Ann. Clin. Microbiol. Antimicrob. 2011, 10: 8. doi:10.1186/1476-0711-10-8. 
  5. ^ Matu M. N., Orinda G. O., Njagi E. N. M., Cohen C. R., Bukusi E. A. In vitro inhibitory activity of human vaginal lactobacilli against pathogenic bacteria associated with bacterial vaginosis in Kenyan women. Anaerobe. 2010, 16: 210–215. doi:10.1016/j.anaerobe.2009.11.002. 
  6. ^ Skarin A., Sylwan J. Vaginal Lactobacilli inhibiting growth of Gardnerella vaginalis, Mobiluncus and other bacterial species cultured from vaginal content of women with bacterial vaginosis. APMIS. 1986, 94: 399–403. doi:10.1111/j.1699-0463.1986.tb03074.x. 
  7. ^ Strus, M., M. Malinowska, and P. B. Heczko. 2002. In vitro antagonistic effect of Lactobacillus on organisms associated with bacterial vaginosis. J. Reprod. Med. 47:41–46.
  8. ^ Boris S., Barbes C. Role played by lactobacilli in controlling the population of vaginal pathogens. Microb. Infect. 2000, 2: 543–546. doi:10.1016/s1286-4579(00)00313-0. 
  9. ^ 9.0 9.1 9.2 Martin R., Suarez J. E. Biosynthesis and degradation of H2O2 by vaginal lactobacilli. Appl. Environ. Microbiol. 2010, 76: 400–405. 
  10. ^ 10.0 10.1 10.2 10.3 10.4 10.5 O'Hanlon D., Moench T., Cone R. In vaginal fluid, bacteria associated with bacterial vaginosis can be suppressed with lactic acid but not hydrogen peroxide. BMC Infect. Dis. 2011, 11: 200. doi:10.1186/1471-2334-11-200. 
  11. ^ Aroutcheva A.; Gariti D.; Simon M.; Shott S.; Faro J.; Simoes J. A.; Gurguis A.; Faro S. Defense factors of vaginal lactobacilli. Am. J. Obstet. Gynecol. 2001, 185: 375–379. 
  12. ^ Linhares I. M., Summers P. R., Larsen B., Giraldo P. C., Witkin S. S. Contemporary perspectives on vaginal pH and lactobacilli. Am. J. Obstet. Gynecol. 2011, 204: 120.e1–120.e5. doi:10.1016/j.ajog.2010.07.010. 
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