title: Individual acid aspartic proteinases (Saps) 1-6 of Candida albicans are not essential for invasion and colonization of the gastrointestinal tract in mice.
abstract: In order to investigate whether there is a role for individual secreted aspartic proteinases (Saps) of Candida albicans in gastrointestinal infection of mice we compared the differential expression of SAP1-6 genes and production of Sap1-6 proteins with invasion and persistence of SAP knockout strains in the gastrointestinal tract. Using an in vivo expression technology (IVET) we found a high percentage of expression of SAP4-6 genes which increased steadily in the course of infection. Expression of SAP1-3 genes was detected occasionally and in lower percentages than that of SAP4-6 genes. With reverse transcriptase-polymerase chain reaction (RT-PCR), mRNA for SAP 4 and SAP6 were detected in the stomach of all mice, whereas SAP2, SAP3 and SAP5 mRNA were detected not in all animals and SAP1 mRNA was not detectable. Also with immunoelectron microscopy we demonstrated production of Saps1-3 as well as Saps4-6 with antibodies cross-reacting with either Saps1-3 or Saps4-6. In contrast to the fact that gene expression and production of Saps were readily detectable, we were unable to demonstrate differences in the ability to invade the stomach, to disseminate to the brain as well as in the duration of faecal shedding and the number of fungi persisting in the faeces of mice infected with SAP knockout strains in comparison to control strains. We conclude that although Saps were produced, individual Saps were not indispensable factors for virulence during gastrointestinal infection of mice.
authors.affiliation: Institut für Medizinische Mikrobiologie und Hygiene, Fakultät für Klinische Medizin Mannheim der Universität Heidelberg, Theodor-Kutzer-Ufer 1-3, D-68167 Mannheim, Germany.
authors.forename: Marianne
authors.initials: M
authors.lastname: Kretschmar
authors.forename: Angelika
authors.initials: A
authors.lastname: Felk
authors.forename: Peter
authors.initials: P
authors.lastname: Staib
authors.forename: Martin
authors.initials: M
authors.lastname: Schaller
authors.forename: Daniela
authors.initials: D
authors.lastname: Hess
authors.forename: Melvin
authors.initials: M
authors.lastname: Callapina
authors.forename: Joachim
authors.initials: J
authors.lastname: Morschhäuser
authors.forename: Wilhelm
authors.initials: W
authors.lastname: Schäfer
authors.forename: Hans Christian
authors.initials: HC
authors.lastname: Korting
authors.forename: Herbert
authors.initials: H
authors.lastname: Hof
authors.forename: Bernard
authors.initials: B
authors.lastname: Hube
authors.forename: Thomas
authors.initials: T
authors.lastname: Nichterlein
mesh_terms: D000818:Animals; D016282:Aspartic Acid Endopeptidases / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D002176:Candida albicans / Q000201:enzymology* / Q000235:genetics / Q000254:growth & development; D002177:Candidiasis / Q000201:enzymology / Q000382:microbiology* / Q000473:pathology; D018076:DNA, Complementary / Q000737:chemistry; D005260:Female; D005767:Gastrointestinal Diseases / Q000201:enzymology / Q000382:microbiology* / Q000473:pathology; D015966:Gene Expression Regulation, Fungal; D006651:Histocytochemistry; D016867:Immunocompromised Host; D007413:Intestinal Mucosa / Q000382:microbiology / Q000473:pathology; D007527:Isoenzymes / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology; D051379:Mice; D008807:Mice, Inbred BALB C; D016253:Microscopy, Immunoelectron; D012333:RNA, Messenger / Q000737:chemistry / Q000302:isolation & purification; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013047:Specific Pathogen-Free Organisms; D013270:Stomach / Q000382:microbiology / Q000473:pathology
chemical_list: D018076:DNA, Complementary; D007527:Isoenzymes; D012333:RNA, Messenger; D016282:Aspartic Acid Endopeptidases