title: Specific inhibition of Candida albicans growth in vitro by antibodies from experimental Candida keratitis mice.
abstract: To investigate the role of humoral immunity in the response to experimental keratitis, Balb/c mice were primed by one of three protocols: i) intranasal inhalation of live Candida spores; ii) subcutaneous injection of heat-inactivated spores; or iii) induction and healing of primary CaK. Experimental murine CaK was then induced in the three groups of primed mice and one group of unprimed mice by intrastromal injection of live Candida albicans spores. Totally 30 mice were included in each group. Sera collected after CaK induction were subjected to serial dilution and their effects on fungal growth and survival were tested as an assay for fungicidal activity in vitro. Corneas removed at various stages of disease were examined histologically, and fungal loads were determined using quantitative real-time PCR. Compared to corneas from mice with primary CaK, all corneas from CaK mice that had been previously primed exhibited milder histological disruptions that were faster to resolve, contained higher immunoglobulin and IFNγ titers, and had lower pathogen load (P < 0.05). Infiltration of pro-Inflammatory cells, which comprised mainly leukocytes other than lymphocytes, also initiated earlier in the primed mice compared to the controls (at day 3 versus day 7 respectively), and this should be due to differential production of cytokines. Sera from primed CaK mice exhibited stronger fungicidal activity and this was relatively specific for the original pathogen. Based on these findings, we proposed that the humoral response elicited by CaK plays important role in host protection against secondary C. albicans infections, and this might be achieved by pathogen-specific inhibition of fungal survival and/or growth.
authors.affiliation: Shandong Provincial Key Laboratory of Ophthalmology, Shandong Eye Institute, Shandong Academy of Medical Sciences, 5 Yanerdao Road, Qingdao 266071, China.
authors.forename: Hongbo
authors.initials: H
authors.lastname: Zhang
authors.forename: Changkai
authors.initials: C
authors.lastname: Jia
authors.forename: Haijie
authors.initials: H
authors.lastname: Xi
authors.forename: Siyuan
authors.initials: S
authors.lastname: Li
authors.forename: Lingling
authors.initials: L
authors.lastname: Yang
authors.forename: Yiqiang
authors.initials: Y
authors.lastname: Wang
mesh_terms: D000818:Animals; D000908:Antibodies, Fungal / Q000494:pharmacology*; D000920:Antibody-Dependent Cell Cytotoxicity / Q000502:physiology; D002176:Candida albicans / Q000187:drug effects* / Q000276:immunology*; D002177:Candidiasis / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D003114:Colony-Forming Units Assay; D003315:Cornea / Q000378:metabolism / Q000382:microbiology; D003320:Corneal Ulcer / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D004797:Enzyme-Linked Immunosorbent Assay; D015821:Eye Infections, Fungal / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D056724:Immunity, Humoral / Q000502:physiology; D007070:Immunoglobulin A / Q000276:immunology; D007074:Immunoglobulin G / Q000276:immunology; D007371:Interferon-gamma / Q000378:metabolism; D015847:Interleukin-4 / Q000378:metabolism; D008214:Lymphocytes / Q000502:physiology; D051379:Mice; D008807:Mice, Inbred BALB C; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D000908:Antibodies, Fungal; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D015847:Interleukin-4; D007371:Interferon-gamma