Identification of Candida albicans regulatory genes governing mucosal infection

2018 ◽  
Vol 20 (8) ◽  
Author(s):  
Juliane Meir ◽  
Elena Hartmann ◽  
Marie‐Therese Eckstein ◽  
Eva Guiducci ◽  
Florian Kirchner ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Regulatory Genes ◽  
Mucosal Infection

scholarly journals Oral candidiasis-adhesion of non-albicans Candida species

2008 ◽  
pp. 69-78 ◽  
Author(s):  
Marija Bokor-Bratic
Keyword(s):  
Candida Albicans ◽  
Candida Species ◽  
Oral Candidiasis ◽  
Initial Step ◽  
Oral Microflora ◽  
Mucosal Surfaces ◽  
Buccal Epithelial Cells ◽  
Mucosal Infection ◽  
Denture Acrylics ◽  
Candida Colonisation

Oral candidiasis is an opportunistic infection caused primarily by Candida albicans. However, in recent years, species of non-albicans Candida have been implicated more frequently in mucosal infection. Candida species usually reside as commensal organisms and are part of normal oral microflora. Determining exactly how transformation from commensal to pathogen takes place and how it can be prevented is continuous challenge for clinical doctors. Candidal adherence to mucosal surfaces is considered as a critical initial step in the pathogenesis of oral candidiasis. Acrylic dentures, acting as reservoirs, play an important role in increasing the risk from Candida colonisation. Thus, this review discusses what is currently known about the adhesion of non-albicans Candida species of oral origin to buccal epithelial cells and denture acrylics.

scholarly journals IL-12 and Related Cytokines: Function and Regulatory Implications inCandida albicansInfection

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Robert B. Ashman ◽  
Dipti Vijayan ◽  
Christine A. Wells
Keyword(s):  
Candida Albicans ◽  
Adaptive Immunity ◽  
Adaptive Response ◽  
Systemic Disease ◽  
Oral Infection ◽  
Innate And Adaptive Immunity ◽  
Cytokine Responses ◽  
Mucosal Infection ◽  
Disseminated Disease

IL-12 is a cytokine with links to both innate and adaptive immunity systems. In mice, its deletion leads to acute susceptibility to oral infection with the yeastCandida albicans, whereas such mice are resistant to systemic disease. However, it is an essential component of the adaptive response that leads to the generation of Th1-type cytokine responses and protection against disseminated disease. This paper presents an overview of the role of IL-12 in models of systemic and mucosal infection and the possible relationships between them.

scholarly journals Penatalaksanaan kandidiasis oral disebabkan Candida tropicalis pada anak dengan gangguan sistemik

2010 ◽  
Vol 9 (2) ◽  
pp. 78
Author(s):  
Cane Lukisari ◽  
Dwi Setyaningtyas ◽  
Mintarsih Djamhari
Keyword(s):  
Candida Albicans ◽  
Incidence Rate ◽  
Candida Tropicalis ◽  
Oral Candidiasis ◽  
Supportive Therapy ◽  
Good Prognosis ◽  
Oral Infection ◽  
Mucosal Infection ◽  
Adherence Ability

Oral candidiasis is an oral mucosal infection caused by Candida albicans (CA) ornon-Candida albicans Candida (NCAC). C. tropicalis (CT) is most virulent NCACbecause it has the most adherence ability to epithelial cells in vitro as well as mediumlevel proteinase secretion. In addition, CT is the second most common colony found inhuman. Although incidence rate of oral infection was low, this species has virulencepotency, lately reported as the mayor cause of candidemia in immunocompromisedpatients. This paper reports and discusses oral candidiasis due to CT in a child whosuffered anemia with clinical sign of malnutrition. Oral nystatin suspension is therapyof choice because of patient well response, and in vitro studies reported lack ofresponse of fluconazole to candidemia due to C.tropicalis. However, nystatin oralsuspension, should be synchronized with hygiene optimalization of elimination ofpredisposition factors, and supportive therapy would provide a good prognosis.

scholarly journals ERG3 and ERG11 genes are critical for the pathogenesis of Candida albicans during the oral mucosal infection

2018 ◽  
Vol 10 (2) ◽  
Author(s):  
Yujie Zhou ◽  
Min Liao ◽  
Chengguang Zhu ◽  
Yao Hu ◽  
Ting Tong ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Mucosal Infection

scholarly journals Development of an Orogastrointestinal Mucosal Model of Candidiasis with Dissemination to Visceral Organs

2006 ◽  
Vol 50 (8) ◽  
pp. 2650-2657 ◽  
Author(s):  
Karl V. Clemons ◽  
Gloria M. Gonzalez ◽  
Gaurav Singh ◽  
Jackie Imai ◽  
Marife Espiritu ◽  
...  
Keyword(s):  
Small Intestine ◽  
Candida Albicans ◽  
Drug Efficacy ◽  
Oral Infection ◽  
Cytotoxic Chemotherapy ◽  
Antibacterial Treatment ◽  
Developmental Studies ◽  
Mucosal Infection ◽  
Mucosal Candidiasis ◽  
Disseminated Disease

ABSTRACT Studies were done to develop a murine model that mimics the pattern of mucosal candidiasis followed by disseminated disease seen in patients given cytotoxic chemotherapy. Developmental studies showed that suppression of mice with 5-fluorouracil beginning 3 days prior to infection and given every 7 days thereafter necessitated antibacterial treatment but resulted in a reproducible model. Candida albicans given in the drinking water resulted in oral infection by day 3 that significantly increased from days 10 to 15 and mucosal infection with 4 to 7 log10 Candida CFU in the esophagus, stomach, small intestine, and cecum. Dissemination to livers occurred and was 100% on days 5 to 15; fewer animals had kidney infection. The median kidney or liver CFU were 2 or 3 log10 CFU, respectively, on day 15; despite this, mortality was low through 21 days of infection. As a demonstration of the utility of the model to test antifungal activity, daily treatment with 10 or 50 mg/kg itraconazole significantly reduced dissemination to the liver and kidneys and reduced tongue CFU compared to controls. Overall, these studies indicate that a nonlethal model of oral and gastrointestinal mucosal candidiasis with dissemination can be established in mice. Drug efficacy in treating localized infection and in preventing or treating disseminated infection can be studied.

scholarly journals The Interactions Between Candida albicans and Mucosal Immunity

2021 ◽  
Vol 12 ◽  
Author(s):  
Yujie Zhou ◽  
Lei Cheng ◽  
Yu L. Lei ◽  
Biao Ren ◽  
Xuedong Zhou
Keyword(s):  
Candida Albicans ◽  
Mucosal Immunity ◽  
Cytokine Production ◽  
Immune Cell ◽  
Fungal Infections ◽  
Immune Defense ◽  
The Body ◽  
Pathogen Invasion ◽  
Mucosal Infection ◽  
And Control

Mucosa protects the body against external pathogen invasion. However, pathogen colonies on the mucosa can invade the mucosa when the immunosurveillance is compromised, causing mucosal infection and subsequent diseases. Therefore, it is necessary to timely and effectively monitor and control pathogenic microorganisms through mucosal immunity. Candida albicans is the most prevalent fungi on the mucosa. The C. albicans colonies proliferate and increase their virulence, causing severe infectious diseases and even death, especially in immunocompromised patients. The normal host mucosal immune defense inhibits pathogenic C. albicans through stepwise processes, such as pathogen recognition, cytokine production, and immune cell phagocytosis. Herein, the current advances in the interactions between C. albicans and host mucosal immune defenses have been summarized to improve understanding on the immune mechanisms against fungal infections.

scholarly journals Processing of Candida albicans Ece1p Is Critical for Candidalysin Maturation and Fungal Virulence

mBio ◽  
2018 ◽  
Vol 9 (1) ◽  
Author(s):  
Jonathan P. Richardson ◽  
Selene Mogavero ◽  
David L. Moyes ◽  
Mariana Blagojevic ◽  
Thomas Krüger ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Amino Acid ◽  
Fungal Pathogen ◽  
Fungal Virulence ◽  
Epithelial Damage ◽  
Mucosal Infection ◽  
Peptide Toxin ◽  
Opportunistic Fungal Pathogen ◽  
Factor C

ABSTRACTCandida albicansis an opportunistic fungal pathogen responsible for superficial and life-threatening infections in humans. During mucosal infection,C. albicansundergoes a morphological transition from yeast to invasive filamentous hyphae that secrete candidalysin, a 31-amino-acid peptide toxin required for virulence. Candidalysin damages epithelial cell plasma membranes and stimulates the activating protein 1 (AP-1) transcription factor c-Fos (via p38–mitogen-activated protein kinase [MAPK]), and the MAPK phosphatase MKP1 (via extracellular signal-regulated kinases 1 and 2 [ERK1/2]–MAPK), which trigger and regulate proinflammatory cytokine responses, respectively. The candidalysin toxin resides as a discrete cryptic sequence within a larger 271-amino-acid parental preproprotein, Ece1p. Here, we demonstrate that kexin-like proteinases, but not secreted aspartyl proteinases, initiate a two-step posttranslational processing of Ece1p to produce candidalysin. Kex2p-mediated proteolysis of Ece1p after Arg61 and Arg93, but not after other processing sites within Ece1p, is required to generate immature candidalysin from Ece1p, followed by Kex1p-mediated removal of a carboxyl arginine residue to generate mature candidalysin.C. albicansstrains harboring mutations of Arg61 and/or Arg93 did not secrete candidalysin, were unable to induce epithelial damage and inflammatory responsesin vitro, and showed attenuated virulencein vivoin a murine model of oropharyngeal candidiasis. These observations identify enzymatic processing ofC. albicansEce1p by kexin-like proteinases as crucial steps required for candidalysin production and fungal pathogenicity.IMPORTANCECandida albicansis an opportunistic fungal pathogen that causes mucosal infection in millions of individuals worldwide. Successful infection requires the secretion of candidalysin, the first cytolytic peptide toxin identified in any human fungal pathogen. Candidalysin is derived from its parent protein Ece1p. Here, we identify two key amino acids within Ece1p vital for processing and production of candidalysin. Mutations of these residues renderC. albicansincapable of causing epithelial damage and markedly reduce mucosal infectionin vivo. Importantly, candidalysin production requires two individual enzymatic events. The first involves processing of Ece1p by Kex2p, yielding immature candidalysin, which is then further processed by Kex1p to produce the mature toxin. These observations identify important steps forC. albicanspathogenicity at mucosal surfaces.

Enhanced IgE response to Candida albicans in postoperative invasive candidiasis

1996 ◽  
Vol 26 (4) ◽  
pp. 452-460 ◽  
Author(s):  
J. SAVOLAINEN ◽  
A. RANTALA ◽  
M. NERMES ◽  
L. LEHTONEN ◽  
M. VIANDER
Keyword(s):  
Candida Albicans ◽  
Invasive Candidiasis ◽  
Ige Response

Existence of Candida albicans and microorganisms in denture stomatitis patients

1997 ◽  
Vol 24 (10) ◽  
pp. 788-790 ◽  
Author(s):  
Y. KULAK ◽  
A. ARIKAN ◽  
E. KAZAZOGLU
Keyword(s):  
Candida Albicans ◽  
Denture Stomatitis
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