|
| ||
|
|
||
Candida Albicans Infection (candida + albican_infection)
Selected AbstractsDifferential role of IL-18 and IL-12 in the host defense against disseminated Candida albicans infectionEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 12 2003Mihai Abstract IFN-, plays a crucial role in the defense against infection with Candida albicans. Since IL-18 and IL-12 are strong stimuli of IFN-, production, we investigated whether endogenous IL-18 and IL-12 are involved in the host defense during disseminated candidiasis. IL-18 knockout (IL-18-/-) mice, but not IL-12-/- mice, displayed an increased mortality due to C. albicans infection, accompanied by a decreased clearance of the yeasts from the kidneys late during the course of infection. Histopathology of the organs, combined with phagocyte recruitment experiments, showed a decreased influx of monocytes at the sites of Candida infection, mainly in the IL-18-/- mice. Whereas production of the chemokine KC was decreased in both IL-18-/- and IL-12-/- mice, MIP-2 production was deficient only in IL-18-/- animals, which may explain the differences in phagocyte recruitment. In addition, although IFN-, production capacity, as a parameter of the Th1-protective immunity, was reduced by 65 to 80% in the IL-12-/- mice, this defect was even more pronounced in the IL-18-/- mice (85 to 95% downmodulation). In conclusion, the anticandidal effects of endogenous IL-18 are mediated late during the infection by assuring a proper IFN-, response and promoting the infiltration of the site of infection by monocytes. [source] Enhanced resistance against systemic Candida albicans infection in mice treated with C. albicans DNAFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 2 2008Petya Dimitrova Abstract In this study, double-stranded Candida albicans DNA was administered in systemic C. albicans infection in at dose of 20 ,g per mouse at 4, 5 and 6 weeks of age. The level of IL-12 in serum was elevated as a result of yeast DNA treatment and correlated with lower mortality and decreased kidney and liver injury. Macrophage activation was demonstrated by an increase of nitric oxide (NO) and IL-12 production. These effects were Janus activation kinases (JAK)/signal transducer and activator of transcription (STAT) dependent as they were inhibited by selective JAK inhibitor tyrphostin AG-490. DNA influenced adaptive immune response through elevation of anti- Candida IgG antibody production in systemic C. albicans infection. Thus, C. albicans DNA augmented innate and adaptive immune responses against the pathogen. [source] CpG oligodeoxynucleotides protect mice from lethal challenge with Candida albicans via a pathway involving tumor necrosis factor-,-dependent interleukin-12 inductionFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 1 2007Jung-Hwa Choi Abstract In this study, we have attempted to determine whether the systemic administration of CpG oligodeoxynucleotide (CpG-ODN) 1826 would protect mice against systemic lethal Candida albicans infection. CpG-ODNs were found completely to protect mice from death and also reduced the growth of C. albicans in the kidneys. The administration of CpG-ODNs resulted in early interleukin (IL)-12 mRNA expression in the kidneys and an increase in serum IL-12 levels. The protective activity of CpG-ODN was abolished in IL-12-deficient (IL-12,/,) mice, thereby indicating the IL-12-dependency inherent to the effects of CpG-ODN. The protective effect of CpG-ODN was not associated with the activity of NF-,B. Interestingly, in tumor necrosis factor (TNF)-,-deficient (TNF,/,) mice CpG-ODN neither exerted protective effects nor induced IL-12 expression. These data indicate that CpG-ODN protects animals against lethal C. albicans challenge via a pathway that involves the TNF-,-dependent induction of IL-12. [source] Induction of salivary antibodies to inhibit Candida albicans adherence to human epithelial cells by tonsillar immunization in rabbitsFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 3 2006Takaki Fukuizumi Abstract To examine the possibility of a vaccine for Candida albicans infection in the oral cavity, we induced salivary antibodies by immunization of killed- C. albicans ATCC 18804 on the palatine tonsils of rabbits. The enzyme-linked immunosorbent assay reaction of salivary antibodies was high against C. albicans serotype A. The saliva antibodies greatly inhibited C. albicans adherence to cloned epithelial cells from human gingiva. Tonsillar immunizations of C. albicans ATCC 18804 induce salivary antibodies that prevent C. albicans adherence to epithelial cells, and thus should prove useful in the prevention of oral candidiasis caused by C. albicans serotype A. [source] Co-administration of immunomodulator tuftsin and liposomised nystatin can combat less susceptible Candida albicans infection in temporarily neutropenic miceFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 3 2004Masood A Khan Abstract In order to develop a prospective chemotherapeutic agent against opportunistic infections, it is important to know that host factors such as degree of immunological debility as well as recovery of immune functions to normality may contribute significantly to a successful elimination of the pathogens. We demonstrated previously that concomitant delivery of antimicrobial agents and immunomodulators to the pathogen harbouring-host contributes to the complete elimination of the deep-seated fungal infections (aspergillosis and candidiasis) in animals with normal immune status. Considering that neutropenic hosts are the main targets of such infections, it can be argued about the potential of the immunomodulator-based therapy in subjects with non-functional immune system. To resolve the hypothesis, we studied the role of immunomodulator tuftsin against experimental murine candidiasis in temporarily neutropenic Balb/c mice. The neutropenic mice were challenged with an isolate of Candida albicans that was showing less susceptibility to both free and liposomised-amphotericin B. The co-administration of tuftsin increased the efficiency of liposomised-polyene antibiotics (nystatin and amphotericin B) against experimental murine candidiasis in immunocompromised Balb/c mice. Pretreatment with liposomised tuftsin prior to C. albicans infection clearly enhanced protection against candidiasis, suggesting a prophylactic role of tuftsin in normal and temporarily neutropenic animals. [source] Temporal events in the intravenous challenge model for experimental Candida albicans infections in female miceMYCOSES, Issue 3 2005Donna M. MacCallum Summary We characterized the intravenous (i.v.) challenge model for disseminated Candida albicans infection in female BALB/c and DBA/2 mice. Clearance of fungi from the bloodstream and appearance of fungi in tissues were measured at intervals after challenge with various doses of C. albicans. The wild-type isolate SC5314 and derived strains CAF2,1 and CAI-4 transformed with CIp10 were of equal virulence in the model. Variability in mouse survival times, kidney fungal burdens and cachexia was lowest when challenge inocula were within the range 104,105 CFU g,1 body weight in BALB/c mice, but brain fungal burdens and outcomes in DBA/2 mice were variable for all inocula tested. Critical times in the development of infections in optimally challenged BALB/c mice were at 5,10 h (bloodstream fully cleared of fungi), 24 h (start of exponential fungal growth in kidneys) and 48 h (50% of blood cultures become positive). Differential involvement of right and left kidneys occurred almost exclusively in mice challenged with <2 × 104 CFU g,1. We conclude that the i.v. challenge model in female BALB/c mice is now sufficiently well characterized to permit more refined experimentation in future virulence studies with C. albicans mutants. [source] Role of cytokines of the tumour necrosis factor family in the immune response to disseminated Candida albicans infectionBRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 7 2000M. G. Netea Background Tumour necrosis factor (TNF) ,, lymphotoxin (LT) ,, CD40L and FasL are members of the TNF family that play a crucial role in modulation of the immune response. Their role in the defence against infection with Candida albicans was investigated in mice deficient in either TNF-, and LT-, (TNF,/, LT,/, mice), CD40L (CD40L,/, mice) or Fas (MRL/lpr mice). Methods Mortality rates were compared in mice infected intravenously with 106 colony-forming units of C. albicans per mouse. Results After infection with C. albicans the TNF,/, LT,/, mice had a significantly increased mortality rate compared with control mice (100 versus 40 per cent; P < 0·01). This was due to a 10,1000-fold increased outgrowth of the yeasts in the kidneys and liver of TNF,/, LT,/, mice (P < 0·01). Defective recruitment and phagocytosis, but not Candida killing, were responsible for these effects. CD40L,/, mice were also more susceptible to systemic candidiasis than the wild-type controls (mortality rate 80 versus 50 per cent; P < 0·05), and the growth of Candida in the kidneys was one order of magnitude higher in the deficient than in control mice (P < 0·05). Neutrophil function in the CD40L,/, mice was normal, whereas decreased Candida killing by macrophages through nitric oxide-dependent mechanisms was responsible for the effect of CD40/CD40L interactions. In contrast, Fas-defective MRL/lpr mice were significantly more resistant to disseminated candidiasis (mortality rate 50 versus 100 per cent; P < 0·01); this was mediated by the facilitation of neutrophil migration to the site of infection. Conclusion Cytokines of the TNF family play a crucial role in the modulation of host defence against fatal C. albicans infection. Their effects are exerted selectively at the level of neutrophil or macrophage function. © 2000 British Journal of Surgery Society Ltd [source] | ||||||||||