Immunohistochemical study of the vaginal inflammatory response in experimental trichomoniasis.
In the present paper, the acute and subchronical inflammatory processes of the vaginal epithelial were studied in mice experimentally infected with two Trichomonas vaginalis strains of different pathogenicity, by means of histological and immunological methods. There was an increase in the stratified epithelium layers as well as edema produced by the increase of vascularization in the propia submucosa and infiltration of leukocytes. The proliferation of the vaginal epithelium favors the settlement and persistence of the parasitic infection. All of the findings corresponded with signs of a systemic disease being observed in the animals, including significant weight loss and also intestinal invasion. The entire inflammatory process has been corroborated by studies of adhesion molecules such as E-Selectin, VCAM-1 and PECAM-1. A correlation between the time of appearance and the perseverance of the inflammatory process with E-Selectin and VCAM-1 expression was observed, but not with PECAM-1. The strain with a higher pathogenicity was able to invade deep vaginal tissues and thus, parasites could not be detected by vaginal washings. This may be an important cause of diagnosis and treatment failure. Also, by the different localization of trichomonads, it appeared that the battle between host and parasite took place in different areas dependent upon the characteristics of the strain.
Escario
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A
Biolab S.L., Colmenar Viejo, Madrid, Spain.
Gómez Barrio
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A
Simons Diez
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B
Escario
J A
JA
D000818:Animals; D001835:Body Weight; D049109:Cell Proliferation; D004195:Disease Models, Animal; D004848:Epithelium / Q000473:pathology; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007249:Inflammation / Q000473:pathology; D007422:Intestines / Q000469:parasitology; D051379:Mice; D008853:Microscopy; D009092:Mucous Membrane / Q000473:pathology; D014247:Trichomonas Vaginitis / Q000473:pathology*; D014246:Trichomonas vaginalis / Q000472:pathogenicity*