Antitrichomonas IgG, IgM, IgA, and IgG subclass responses in human intravaginal trichomoniasis

Abstract

Trichomoniasis, caused by the protozoan parasite Trichomonas vaginalis, is a major nonviral sexually transmitted disease. Clinical spectrum varies from an asymptomatic state to mild, moderate, or severe symptoms. However, the exact factors leading to the variations in symptoms have not been well elucidated. Host's immune response to the parasite may be playing a role in varied symptomatology. The present study reports antitrichomonas IgM, IgA, IgG and its subclasses in doubling dilutions of serum and diluted vaginal washes of six T. vaginalis-infected symptomatic and four T. vaginalis-infected asymptomatic women and uninfected controls by enzyme-linked immunosorbent assay (ELISA). No significant difference was observed in serum IgG ELISA absorbance values from symptomatic compared to asymptomatic subjects (p > 0.05) while a significant difference (p < 0.05) was noted in serum IgM in all the tested dilutions and IgA up to a dilution of 400. This is the first report of the detection of specific IgG subclass response in T. vaginalis-infected female patients, and quantitative analysis of the antibody responses indicated that the production of local IgG particularly IgG1 in vaginal secretions may be playing a significant role in establishing symptomatic infection. The interesting observation of the present study is that the specific IgM was detected in 2 (33.3%) symptomatic and T. vaginalis-infected patients in > or =800 dilutions and in 1 (16.6%) up to 200 dilutions in serum, while it was not detectable in the vaginal secretions of symptomatic patients or in the serum and vaginal secretions of asymptomatic T. vaginalis-infected patients.

Impact of T. vaginalis infection on innate immune responses and reproductive outcome

“…Both circulating and mucosal antibodies have been detected in women (Kaur et al, 2008); however, the immunity is not lasting, and it has been shown that T. vaginalis cysteine proteases present in the serum and vaginal secretions of symptomatic women can degrade IgG, IgM, and IgA (Yadav et al, 2007). In addition, the T. vaginalis cysteine proteases including CP30, induce apoptosis in vaginal epithelial cells (Sommer et al, 2005) and in multiple mucosal immune cell types (discussed below).…”

Investigation of the presence of Trichomonas vaginalis in infertile Turkish women

“…Antibodies against T. vaginalis were detected in circulation and vaginal mucosa of infected women [8,22,23]. T. vaginalis cysteine proteases including CP30 may induce apoptosis of vaginal epithelial cells and multiple mucosal immune cell types [8,24].…”

Immunity to Sexually Transmitted Infections

“…Although human infection with T. vaginalis induces antibody responses (Fichorova et al, 2006;Kaur et al, 2008), repeated infections can occur, suggesting that innate defenses may be more important (Fichorova, 2009). Greater serum and vaginal IgA antibody responses and increased IFN-γ, IL-2, and TNF-α responses have been reported in mice infected with T. vaginalis isolates derived from asymptomatic women compared to those from symptomatic women (Paintlia et al, 2002).…”