Budrys NM, Gong S, Rodgers AK, Wang J, Louden C, Shain R, Schenken RS, Zhong G

Budrys NM, Gong S, Rodgers AK, Wang J, Louden C, Shain R, Schenken RS, Zhong G. laid a foundation for further revealing the mechanisms by which is a leading infectious cause of infertility due to its ability to induce tubal inflammation/adhesion/fibrosis/hydrosalpinx in women (1,C4). However, the mechanisms by which induces long-term sequelae in the upper genital tract remain unclear. The mouse-adapted species has been used to investigate pathogenesis because of its ability to induce long-lasting tubal fibrosis/hydrosalpinx in mice (5,C9). Following intravaginal inoculation, ascends to the oviduct to induce tubal inflammation (10) that may both clear chlamydial infection and damage tubal epithelia, triggering tissue-repairing responses, including transient fibrosis. In many cases, mouse tubal fibrosis continues despite Pipemidic acid the clearance of the initial chlamydial infection, leading to oviduct lumen occlusion/hydrosalpinx/infertility (5, 7, 9). The mouse model with induction of hydrosalpinx has been Pipemidic acid useful for investigating chlamydial pathogenic mechanisms. Pipemidic acid For example, a chlamydial plasmid was found to be an important pathogenic determinant since depleted of the plasmid was no longer able to induce hydrosalpinx (11,C14). It was also found that mouse CD8+ T cells promoted (15, 16) while CD4+ T cells prevented (17) induction of hydrosalpinx. However, it remains unknown why and how long-lasting tubal fibrosis is still maintained Mouse monoclonal to CD38.TB2 reacts with CD38 antigen, a 45 kDa integral membrane glycoprotein expressed on all pre-B cells, plasma cells, thymocytes, activated T cells, NK cells, monocyte/macrophages and dentritic cells. CD38 antigen is expressed 90% of CD34+ cells, but not on pluripotent stem cells. Coexpression of CD38 + and CD34+ indicates lineage commitment of those cells. CD38 antigen acts as an ectoenzyme capable of catalysing multipe reactions and play role on regulator of cell activation and proleferation depending on cellular enviroment long after oviduct infection is cleared. is also routinely detected in the gastrointestinal (GI) tracts of humans (18,C22) and animals (23,C27). imaging of mice (28) revealed that genital spread to and colonized the GI tract for long periods (24). Spreading might occur via blood circulation (24, 26, 29, 30). Systemically disseminated organisms were cleared within 2 to 3 3?weeks, Pipemidic acid and only those that reached the GI tract lumen could persist for long periods (26, 27). Although GI has been hypothesized to serve as a reservoir for autoinoculation of the genital tract lumen to promote chlamydial pathogenicity (25, 31), mice intragastrically (i.g.) inoculated with failed to autoinoculate their genital tract lumen (27) and did not develop any significant pathology in either the genital tract or the GI tract (32, 33). The question was whether in the mouse GI tract could affect the pathogenicity of genital could affect the pathogenicity of genital in mice (34). In coinoculated mice, the contributions of in the genital tract versus the GI tract to the development of hydrosalpinx can be measured separately. This is because although mutants Pipemidic acid such as plasmid-free (Pf) can still ascend to the upper genital tract, they are attenuated in both inducing hydrosalpinx and spreading to the GI tract. Thus, Pf may be able to cause only genital damage without triggering significant responses in the GI tract. Furthermore, intragastrically inoculated wild-type (Wt) is restricted to the GI tract without contaminating the genital tract lumen. Thus, intragastrically inoculated Wt cannot directly cause tissue injury in the genital tract. It was found that although intravaginal inoculation with Pf alone failed to induce hydrosalpinx, intragastric coinoculation with Wt successfully rescued Pf to induce hydrosalpinx. It is worth noting that intragastric coinoculation was applied 1 week after intravaginal inoculation in order to best mimic the kinetics of natural spread and avoid interference of the gastrointestinal responses with the genital infection course (33). Gastrointestinal Wt was restricted to the GI tract without spreading to the genital tract lumen when both Pf and Wt organisms were tracked simultaneously but separately. Thus, gastrointestinal must use an indirect mechanism to promote hydrosalpinx development in the.