Open veterinary journal · 2026
Evaluation of immunological and gene expression responses induced by Galectin-3 and whole-sonicated Candida krusei antigen in rats experimentally infected with Candida krusei.
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Hussein Hussein Ali, Falih Inam Bader
Аннотация
BACKGROUND: Candida krusei is an emerging non-Candida albicans species increasingly associated with antifungal resistance and invasive systemic infections. Galectin-3 (GAL-3), a β-galactosidase-binding lectin, and the surfactant protein D gene are important components of innate antifungal immunity. The chemokine (C-X-C motif) ligand-1 gene plays a central role in neutrophil recruitment, whereas whole-sonicated C. krusei antigen may act as a broad fungal immunogen.
AIM: To evaluate the immunological and pulmonary gene expression responses induced by GAL-3, whole-sonicated C. krusei antigen, and their combination in rats experimentally infected with C. krusei, via measurement of serum immunoglobulin G, interleukin-17, interleukin-23, and lung expression of Chemokine (C-X-C motif) ligand 1 (CXCL-1) and surfactant protein D genes.
METHODS: A total of 120 rats were randomly allocated into four experimental groups (n = 30). Animals received GAL-3, whole-sonicated C. krusei antigen, and their combination, while the control group was subdivided into infected and healthy controls. Immunized groups were administered subcutaneously according to the experimental schedule. Systemic C. krusei infection was induced intraperitoneally, and samples were collected at 15 and 30 days post-challenge. Serum Immunoglobulin G, Interleukin -17 (IL-17), and Interleukin -23 (IL-23) levels were measured using ELISA. Pulmonary CXCL-1 and surfactant protein D gene expression were quantified using SYBR Green reverse transcription quantitative polymerase chain reaction and analyzed using the 2⁻ΔΔCt method.
RESULTS: Immunoglobulin G levels increased significantly in all treated groups compared with infected and healthy controls, with the highest levels at day 30. Whole-sonicated C. krusei antigen and mixed treatment groups showed significant increases in IL-17 and IL-23, indicating activation of Th17-mediated immune responses. Galectin-3 treatment produced upregulation of CXCL-1 and surfactant protein D genes, whereas the antigen-treated group showed moderate gene expression changes. The combined treatment group demonstrated reduced CXCL-1 induction but maintained a modest increase in surfactant protein D expression.
CONCLUSION: Galectin-3 and whole-sonicated C. krusei antigen may enhance antifungal immune responses through partially distinct mechanisms. Galectin-3 modulates the CXCL-1 and surfactant protein D gene axis and activate innate immune pathways, whereas whole-sonicated antigen stimulates IL-23/IL-17-mediated responses and humoral immunity. These findings suggest that GAL-3 and fungal antigen immunization may represent support immunomodulatory approaches for controlling infections caused by non-C. albicans.
AIM: To evaluate the immunological and pulmonary gene expression responses induced by GAL-3, whole-sonicated C. krusei antigen, and their combination in rats experimentally infected with C. krusei, via measurement of serum immunoglobulin G, interleukin-17, interleukin-23, and lung expression of Chemokine (C-X-C motif) ligand 1 (CXCL-1) and surfactant protein D genes.
METHODS: A total of 120 rats were randomly allocated into four experimental groups (n = 30). Animals received GAL-3, whole-sonicated C. krusei antigen, and their combination, while the control group was subdivided into infected and healthy controls. Immunized groups were administered subcutaneously according to the experimental schedule. Systemic C. krusei infection was induced intraperitoneally, and samples were collected at 15 and 30 days post-challenge. Serum Immunoglobulin G, Interleukin -17 (IL-17), and Interleukin -23 (IL-23) levels were measured using ELISA. Pulmonary CXCL-1 and surfactant protein D gene expression were quantified using SYBR Green reverse transcription quantitative polymerase chain reaction and analyzed using the 2⁻ΔΔCt method.
RESULTS: Immunoglobulin G levels increased significantly in all treated groups compared with infected and healthy controls, with the highest levels at day 30. Whole-sonicated C. krusei antigen and mixed treatment groups showed significant increases in IL-17 and IL-23, indicating activation of Th17-mediated immune responses. Galectin-3 treatment produced upregulation of CXCL-1 and surfactant protein D genes, whereas the antigen-treated group showed moderate gene expression changes. The combined treatment group demonstrated reduced CXCL-1 induction but maintained a modest increase in surfactant protein D expression.
CONCLUSION: Galectin-3 and whole-sonicated C. krusei antigen may enhance antifungal immune responses through partially distinct mechanisms. Galectin-3 modulates the CXCL-1 and surfactant protein D gene axis and activate innate immune pathways, whereas whole-sonicated antigen stimulates IL-23/IL-17-mediated responses and humoral immunity. These findings suggest that GAL-3 and fungal antigen immunization may represent support immunomodulatory approaches for controlling infections caused by non-C. albicans.