Innate immunity to infection in the lower female genital tract

被引:7
|
作者
Gregorczyk, Karolina Paulina [1 ]
Krzyzowska, Malgorzata [1 ]
机构
[1] Szkola Glowna Gospodarstwa Wiejskiego Warszawie, Zaklad Immunol, Katedra Nauk Przedklin, Wydzial Med Weterynaryjnej, PL-02786 Warsaw, Poland
关键词
lower female genital tract; innate immunity; neutrophils; epithelial cells; Toll-like receptors; bacterial microflora; TOLL-LIKE RECEPTOR-2; NEISSERIA-GONORRHOEAE; CHLAMYDIA-TRACHOMATIS; DENDRITIC CELLS; BACTERIAL VAGINOSIS; REPRODUCTIVE-TRACT; EPITHELIAL-CELLS; NATURAL-KILLER; ESTROUS-CYCLE; VIRUS TYPE-1;
D O I
10.5604/17322693.1048816
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Due to the contact with the external environment, the lower female genital tract is non-sterile. The innate immune system has evolved many mechanisms to protect vaginal tissues from pathogens at the same time allowing for survival of the comensal flora. Innate immunity in the lower female genital tract undergoes hormonal regulation. Estrogen and progesterone levels also influence the vaginal mucosal epithelium remodeling with the neutrophlis playing a crucial role, as the most numerous leukocytes in the vaginal tissue. Being exposed to the environment, the vaginal epithelium consists a physical barrier for pathogens, but it also shows the presence of MHC class I and pattern recognition receptors. By production of cytokines and chemokines, the vaginal epithelium attracts innate immune cells such as neutrophiles, macrophages, dendritic cells or NK cells. Vaginal comensal flora is another important mechanism of innate immunity by production of lactic acid and hydrogen peroxide, inhibiting pathogen's growth. Disturbances of vaginal microflora can result in pathogenic infections such as bacterial vaginosis or candidosis. Together with herpes genitalis, HPV infection, chlamydiosis, trichomatosis and gonorrhoea, vaginal infections increase the risk of acquiring another sexually transmitted disease, includig HIV due to the impaired mucosal integrity, facilitating for tissue penetration by pathogens and development of local inflammation.
引用
收藏
页码:388 / 401
页数:14
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