Candida and dysbacteriosis: A cytologic, population-based study of 100,605 asymptomatic women concerning cervical carcinogenesis

Abstract

Objective Decreased clearance of apoptotic cells is suggested to be a major pathogenic factor in systemic lupus erythematosus (SLE). The aim of this study was to investigate whether the binding of SLE autoantibodies to apoptotic cells influences the phagocytosis of these cells by macrophages. Methods Apoptosis was induced in a human T cell line (Jurkat) and a keratinocyte cell line (HaCaT) by ultraviolet B irradiation. Binding of purified IgG from 26 SLE patients and 15 healthy controls to apoptotic cells was assessed by flow cytometry and Western blotting. Phagocytosis of IgG‐opsonized apoptotic cells by monocyte‐derived macrophages was assessed by light microscopy. Similar experiments were performed with a monoclonal antibody against SSA/Ro and IgG fractions from 5 patients with Sjögren's syndrome (SS) and 5 patients with rheumatoid arthritis (RA). Results IgG fractions from all 26 SLE patients bound to late apoptotic, but not early apoptotic, cells. IgG fractions isolated from SLE patients with different autoantibody profiles showed comparable levels of binding. IgG fractions from healthy controls did not bind. Opsonization of apoptotic cells with IgG fractions from SLE patients resulted in a significant inhibition of phagocytosis as compared with healthy control IgG fractions. A monoclonal antibody directed against SSA/Ro and IgG isolated from 5 antinuclear antibody (ANA)–positive patients with SS were also able to elicit these effects, whereas IgG from 5 ANA‐negative patients with RA did not. The inhibitory effect of patient IgG was abolished by blocking either the Fcγ receptors (FcγR) or the constant region of IgG, using a specific Fc‐blocking peptide. Conclusion Autoantibodies from SLE patients are able to opsonize apoptotic cells and inhibit their uptake by macrophages via an FcγR‐dependent mechanism.

Bacterial vaginosis as a risk factor for high‐grade cervical lesions and cancer in HIV‐seropositive women

“…The lack of an association observed here for BV with high grade cervical lesions differs from the positive association found in a previous study in an HIV-seropositive population in Finland [10], and in populations from Brazil, Holland, and South Africa, in which HIV-status was unrecorded [7][8][9]14]. Our results are consistent, however, with those from two European studies with HIV status unknown [13,15], and three studies in the US, two with unknown HIV-status [6,12] and one with HIV-seropositive participants [16].…”

“…Although different methods were used to diagnose BV across studies (clinical diagnosis (pH >4.5, positive amine test, positive gram stain, and characteristic vaginal discharge) [9,12,13,15], gram stain [6,16], or from Pap slides [7,8,10,14]), in our view, the disparate association results do not appear to be explained by differences in methods to ascertain BV infection.…”

“…Other factors acting in conjunction with HPV infection are likely involved in promoting the oncogenic capabilities of HPV, leading to the development of cancer. Coinfection of HPV with bacterial vaginosis (BV) has been suggested to advance this process and, for more than 25 years, has been considered a possible risk factor for cervical cancer development [6][7][8][9][10][11][12][13][14][15][16].…”

Scoring System and Management Algorithm Assessing the Role of Survivin Expression in Predicting Progressivity of HPV Infections in Precancerous Cervical Lesions

“…Roeters (2010) found the OR for Chlamydia and Gardnerella in high-grade smears are 7 and 12, respectively, and the OR for Trichomonas was also significantly high. Engberts (2007) reported the OR of Candida is 1.85 for LSIL and 2.0 for HSIL. We found that STIs significantly increases the risk of developing CIN 3.…”

Premenstrual vaginal colonization of Candida and symptoms of vaginitis

“…Some studies suggest that colonization rises in the luteal phase of the menstrual cycle (Engberts et al, 2007;Eschenbach et al, 2000;Odds et al, 1988); consequently, it is often thought to be associated with hormonal changes in the menstrual cycle. Several studies have documented point prevalence of vaginal colonization of Candida spp.…”