Oropharyngeal Candidiasis Research Articles

Neutrophil swarming is crucial for limiting oral mucosal infection by Candida albicans.

Oral mucosal colonization by C. albicans (Ca) is benign in healthy people but progresses to deeper infection known as oropharyngeal candidiasis (OPC) that may become disseminated when combined with immunosuppression. Cortisone use and neutropenia are risk factors for invasive mucosal fungal infections, however the mechanisms are poorly understood. Here we identify in vivo neutrophil functional complexes known as swarms that are crucial for preventing Ca epithelial invasion. Anti-Ly6G antibody treatment impaired swarm formation and increased fungal infection depth confirming the role of neutrophil swarms in limiting Ca invasion. Neutrophil swarm function could be disrupted by administration of resolvins, and required leukotriene B4 receptor 1 (BLT1) expression so that administration of a leukotriene synthesis inhibitor reduced neutrophil swarm size permitting Ca invasion beyond the basement membrane. Cortisone treatment similarly reduced neutrophil swarming behavior and BLT1 expression and delayed expression of epithelial cytokines and chemokines. Thus, swarm structures have an important function in preventing deep invasion by C. albicans within the oral mucosa and represent a mechanism for increased disease severity under immune deficient clinical settings.

Epidermal growth factor receptor signaling governs the host inflammatory response to invasive aspergillosis.

The epidermal growth factor receptor (EGFR) has been identified as an epithelial cell receptor for Mucorales fungi and Candida albicans. Blocking EGFR with small molecule inhibitors reduces disease severity in mouse models of mucormycosis and oropharyngeal candidiasis. In contrast, cases of invasive aspergillosis have been reported in cancer patients who were treated with EGFR inhibitors, suggesting that EGFR signaling may play a protective role in the host defense against this infection. Here, we analyzed transcriptomic data from the lungs of mice with invasive aspergillosis and found evidence that Aspergillus fumigatus infection activates multiple genes that are predicted to function in the EGFR signaling pathway. We also found that A. fumigatus infection activates EGFR in both a human small-airway epithelial (HSAE) cell line and in the lungs of immunosuppressed mice. EGFR signaling in HSAE cells is required for maximal endocytosis of A. fumigatus and for fungal-induced proinflammatory cytokine and chemokine production. In a corticosteroid immunosuppressed mouse model of invasive pulmonary aspergillosis, inhibition of EGFR with gefitinib decreased whole-lung cytokine and chemokine levels and reduced accumulation of phagocytes in the lung, leading to a decrease in fungal killing, an increase in pulmonary fungal burden, and accelerated mortality. Thus, EGFR signaling is required for pulmonary epithelial cells to orchestrate the host innate immune defense against invasive aspergillosis in immunosuppressed hosts.IMPORTANCEWhen A. fumigatus infects the lungs, it invades epithelial cells that line the airways. During this process, the fungus interacts with epithelial cell receptors. This interaction stimulates epithelial cells to endocytose the fungus. It also induces these cells to secrete proinflammatory cytokines and chemokines that recruit phagocytes to the site of infection where they can kill the fungus. Here, we show that in small-airway epithelial cells, the EGFR acts as a sensor for A. fumigatus that triggers the production of chemokines in response to fungal infection. In corticosteroid-immunosuppressed mice, blocking EGFR with the kinase inhibitor gefitinib reduces chemokine production in the lungs. This leads to decreased accumulation of neutrophils and dendritic cells in the lungs, reduced A. fumigatus killing, and increased mortality. These results provide a potential explanation as to why some cancer patients who are treated with EGFR inhibitors develop invasive aspergillosis.

Salivary proteins modulate Candida albicans virulence and may prevent oropharingeal candidiasis.

Oral candidiasis can be presented in different ways due to the virulence factors of its etiology such as Candida albicans that have developed an effective set of these factors that are able to improve its pathogenesis. The role of salivary immunological components in the development of candidiasis can provide insights for the development of new methodologies aiming to control this disease. The aim of this study was to evaluate the antifungal activity of two salivary components, histatin 5 and lactoferrin on C. albicans viability and virulence using a fluconazole resistant C. albicans clinical strain. Results showed that histatin 5 and lactoferrin decreased cell viability, and the cell surface hydrophobicity was increased by 18% in presence of 151µg/mL of histatin 5 but was not altered by lactoferrin. It was observed the reduction of 69.3% in the expression of mannoproteins on C. albicans surface in the presence of 151µg/mL of histatin, but proteolytic activity of serine proteinases was not inhibited by any of the proteins. Histatin 5 altered cell ultrastructure predominantly in the cytoplasmic compartment. However, this peptide does not interfere with mitochondrial function neither in membrane permeability of the yeasts. The association index between C. albicans and epithelial cells was increased by 51% in presence of 151µg/mL of histatin. Results suggest that histatin 5 and lactoferrin affects viability and virulence of C. albicans at physiological levels, and the maintenance of these levels may be essential in the prevention of oropharyngeal candidiasis. Exogenous administration of these proteins may become a therapeutic alternative for resistant strains of C. albicans, circumventing toxicity issues, considering their constitutive features.

Genome sequencing of Enterococcus faecalis strain 13, an oral strain isolated from C57BL/6 mice.

Enterococcus faecalis strain 13 (Ef#13) is a tongue isolate from a C57BL/6 mouse with experimental oropharyngeal candidiasis. Short-read sequencing revealed a genome of 2,767,598 bp with a GC content of 38.4%, and 2,649 genes were predicted.

Formulation and evaluation of medicated lozenges containing the solid dispersion of Clotrimazole /PEG 6000 for the treatment of oral candidiasis

The study aimed to formulate Clotrimazole (CLM) as solid dispersion medicated lozenges with enhanced dissolution for treating oropharyngeal candidiasis. They are suitable for many patients and easy to administer. The study used the solvent evaporation method to prepare solid dispersions of CLM using polyethylene glycol 6000 and polyvinyl pyrrolidone at different drug-to-carrier weight ratios. The study found that PEG 6000, when used at a 1:1 weight ratio, significantly improved the dissolution of CLM. The results of the FTIR studies showed that the drug was dispersed within PEG 6000, and there was no drug interaction with the excipients used in medicated lozenge formulations. A 32-factorial design was used to develop, optimize, and evaluate nine formulations of the solid dispersion of CLM/PEG 6000 medicated lozenges for improved therapeutic outcomes. We fabricated the lozenges using biocompatible polymeric gelling agents (chitosan, methyl cellulose, and sodium alginate) at three different levels (0.5, 1, and 1.5%). All the medicated lozenges were uniform in weight and drug content within USP limits, with complete drug release rates ranging from 10–20 minutes for chitosan and sodium alginate formulations, compared to 60 minutes for methyl cellulose. The results showed that the type of polymer and its concentration significantly impacted drug release. The optimized formulation, F-3, containing 1.5% CH, exhibited a drug release of 100.83% ±0.68 at the end of 10 minutes. It demonstrated significant antifungal activity against Candida albicans (p < 0.05), making it suitable for drug delivery in the oral cavity.

Lactobacillus johnsonii is a dominant Lactobacillus in the murine oral mucosa and has chitinase activity that compromises fungal cell wall integrity.

The interactions between the opportunistic pathogen Candida albicans and resident oral bacteria are particularly crucial in maintaining oral health. Emerging antifungal drug-resistant strains, slow-paced drug discovery, and the risk of side effects can compromise the effectiveness of current treatments available for oropharyngeal candidiasis. This study advances the search for alternative microbiome-targeted therapies in oral fungal infections. We report that Lactobacillus johnsonii strain MT4 prevents the Candida-induced bloom of dysbiotic oral enterococci and reduces oral mucosal lesions in an oropharyngeal candidiasis murine model. We also show that this strain directly compromises the cell wall and reduces fungal metabolic activity, partly due to its chitinase activity.

Synergistic cross-kingdom host cell damage between Candida albicans and Enterococcus faecalis.

The fungus Candida albicans and the Gram-positive bacterium Enterococcus faecalis share mucosal niches in the human body. As opportunistic pathogens, both are found to expand population size during dysbiosis, and can cause severe systemic infections in susceptible individuals. Here, we show that the presence of C. albicans results in increased host cell damage by E. faecalis . Furthermore, E. faecalis aggravates oropharyngeal candidiasis in mice. Increased damage is mediated by enterococcal cytolysin, and involves both physical interaction and altered glucose availability. Physical interaction promotes accumulation of bacteria on host cells, facilitating contact of cytolysin with host cells. Glucose depletion by the metabolic activity of the fungus sensitized host cells to cytolysin. This work illustrates how a complex interplay between fungi and bacteria can result in detrimental consequences for the host.

Epidermal Growth Factor Receptor Signaling Governs the Host Inflammatory Response to Invasive Aspergillosis.

The epidermal growth factor receptor (EGFR) has been identified as an epithelial cell receptor for Mucorales fungi and Candida albicans. Blocking EGFR with small molecule inhibitors reduces disease severity in mouse models of mucormycosis and oropharyngeal candidiasis. In contrast, cases of invasive aspergillosis have been reported in cancer patients who were treated with EGFR inhibitors, suggesting that EGFR signaling may play a protective role in the host defense against this infection. Here, we analyzed transcriptomic data from the lungs of mice with invasive aspergillosis and found evidence that Aspergillus fumigatus infection activates multiple genes that are predicted to function in the EGFR signaling pathway. We also found that A. fumigatus infection activates EGFR in both a human small airway epithelial (HSAE) cell line and in the lungs of immunosuppressed mice. EGFR signaling in HSAE cells is required for maximal endocytosis of A. fumigatus and for fungal-induced proinflammatory cytokine and chemokine production. In a corticosteroid immunosuppressed mouse model of invasive pulmonary aspergillosis, inhibition of EGFR with gefitinib decreased whole lung chemokine levels and reduced accumulation of phagocytes in the lung, leading to a decrease in fungal killing, an increase in pulmonary fungal burden, and accelerated mortality. Thus, EGFR signaling is required for pulmonary epithelial cells to orchestrate the host innate immune defense against invasive aspergillosis in immunosuppressed hosts.

An approach to analyze spatiotemporal patterns of gene expression at single-cell resolution in Candida albicans-infected mouse tongues.

Candida albicans is a fungal pathobiont inhabiting multiple mucosal surfaces of the human body. Immunosuppression, antibiotic-induced microbial dysbiosis, or implanted medical devices can impair mucosal integrity enabling C. albicans to overgrow and disseminate, causing either mucosal diseases such as oropharyngeal candidiasis or life-threatening systemic infections. Profiling fungal genes that are expressed in the infected mucosa or in any other infected organ is paramount to understand pathogenesis. Ideally, these transcript profiling measurements should reveal the expression of any gene at the single-cell level. The resolution typically achieved with current approaches, however, limits most gene expression measurements to cell population averages. The approach described in this report provides a means to dissect fungal gene expression in infected tissues at single-cell resolution.

The Role of Innate Receptor TLR2 in Neutrophil Recruitment in Oropharyngeal Candidiasis (OPC)

The Role of Innate Receptor TLR2 in Neutrophil Recruitment in Oropharyngeal Candidiasis (OPC)

Oropharyngeal candidiasis — interdisciplinary aspects of childhood medicine

Scientific research in recent years has increased the interest of clinicians in the role of microorganisms in maintai­ning health and the occurrence of diseases. In most cases, fungal lesions of the oral mucosa are a manifestation of numerous somatic diseases and the results of their treatment and contri­bute to complications. To write this article, the information was searched ­using the databases Scopus, Web of Science, Med Zine, Pub Med, Google Scholar, the new version of the International Classification of Diseases (ICD-11) and the Standards of Care “Rational use of antibacterial and antifungal drugs for therapeutic and prophylactic purposes” (2023) were taken into account. The review presents data from the world literature on the role of fungal infection in the development of oropharyngeal candidiasis in children, current perspectives on the mechanism of its formation, clinical manifestations and diagnosis. A comparative characterization of the recommendations of national and foreign guidelines and a generalization of retrospective analyzes on the feasibility of prescribing systemic antifungal drugs for candidal lesions of the oral mucosa and possible methods of correction for mycoecological disorders in children are given. In the context of the presented problem, an integrated approach of a primary care physician, dentist and pediatrician to the diagnosis and treatment of oropharyngeal candidiasis in children is recommended. Timely diagnosis of oropharyngeal candidiasis in children, individual selection of antifungal drugs, synbiotics and multicomponent agents based on probiotics should be a priority area of joint work of general practitioners — family physicians, pediatricians and dentists.

Combinatorial actions of IL-22 and IL-17 drive optimal immunity to oral candidiasis through SPRRs.

Oropharyngeal candidiasis (OPC) is the most common human fungal infection, arising typically from T cell immune impairments. IL-17 and IL-22 contribute individually to OPC responses, but here we demonstrate that the combined actions of both cytokines are essential for resistance to OPC. Mice lacking IL-17RA and IL-22RA1 exhibited high fungal loads in esophagus- and intestinal tract, severe weight loss, and symptoms of colitis. Ultimately, mice succumbed to infection. Dual loss of IL-17RA and IL-22RA impaired expression of small proline rich proteins (SPRRs), a class of antimicrobial effectors not previously linked to fungal immunity. Sprr2a1 exhibited direct candidacidal activity in vitro, and Sprr1-3a-/- mice were susceptible to OPC. Thus, cooperative actions of Type 17 cytokines mediate oral mucosal anti-Candida defenses and reveal a role for SPRRs.

Oral Candida in post‐radiotherapy patients with xerostomia/hyposalivation: A narrative review

AbstractObjectiveHead and Neck Cancer (HNC) patients receiving radiotherapy (RT) often suffer from xerostomia and/or hyposalivation. As saliva plays an important antimicrobial and cleansing roles, these patients are at higher risks of opportunistic infections. This narrative review aims to provide an overview of current evidence on oral Candida colonisation and infection in these patients.MethodsA literature review of clinical studies on oral Candida colonisation and candidiasis in HNC patients receiving radiotherapy/chemoradiotherapy was conducted.ResultsMany clinical studies found high levels of Candida colonisation and a substantial proportion of post‐RT HNC patients suffering from oropharyngeal candidiasis (OPC). Importantly, oral Candida could be a reservoir for life‐threatening systemic infection in immunocompromised patients. The rising prevalence of non‐albicans Candida species and drug‐resistant infections has made identification of Candida species and antifungal susceptibility more important. Recent advances in oral microbiome and its interactions with Candida are discussed. This review also offers perspectives on limitations of current evidence and suggestions for future research.ConclusionFurther research to better understand Candida carriage, microbiome, OPC, and xerostomia/hyposalivation post‐RT would aid in devising a more comprehensive long‐term management plan and novel therapeutic approaches for HNC patients to achieve the full benefits of RT while minimising side effects.

Changing Paradigm of Yeast Isolates in HIV-Seropositive Patients with Oropharyngeal Candidiasis (OPC).

Background Oropharyngeal candidiasis (OPC) is a common fungal infection in HIV-seropositive patients. Understanding the spectrum of yeast isolates and their antifungal susceptibility patterns is crucial for effective management. This study aimed to determine the yeast isolates, antifungal susceptibility patterns, and associated factors in HIV-seropositive patients with OPC. Material and methods A prospective observational study was conducted on 350 HIV-seropositive patients attending an Integrated Counselling and Testing Centre (ICTC) at the Indira Gandhi Institute of Medical Sciences (IGIMS), Patna, Bihar. Yeast isolates from oropharyngeal lesions were identified, and their antifungal susceptibility was determined by automated method VITEK 2. Demographic characteristics, highly active antiretroviral therapy (HAART) status, and CD4+ cell count categories were analyzed for associations. Results This study of 350 HIV-seropositive patients revealed that 100 tested positive forCandida, with distinct differences between HAART (n=67) and non-HAART (n=33) groups. HAART patients had a younger age distribution and higher median CD4+ cell counts (350 vs. 250 cells/mm³, U = 175, p < 0.05) compared to non-HAART patients.Candida albicanswas the most common species in both groups, but significant variations in species distribution (χ² = 9.23, p < 0.05) and antifungal susceptibility were noted. Specifically, susceptibility differences were significant for flucytosine (χ² = 7.21, p = 0.027) and voriconazole (χ² = 8.64, p = 0.013), emphasizing the influence of HAART on managing immune function and antifungal resistance in HIV patients. Conclusion This study provides insights into the spectrum of yeast isolates and their antifungal susceptibility patterns in HIV-seropositive patients with OPC. The findings emphasize the importance of considering multiple factors, such asCandida species, HAART status, and individual patient characteristics, in treatment decisions. The results will aid in the development of evidence-based management protocols for this vulnerable population. Further research is warranted to explore additional factors influencing antifungal susceptibility and optimize treatment strategies for this patient population.

Fungalvaccines and adjuvants: atooltorevealtheinteractionbetweenhostandfungi.

Fungal infections are incurring high risks in a range from superficial mucosal discomforts (such as oropharyngeal candidiasis and vulvovaginal candidiasis) to disseminated life-threatening diseases (such as invasive pulmonaryaspergillosis and cryptococcal meningitis) and becoming a global health problem in especially immunodeficient population. The major obstacle to conquer fungal harassment lies in the presence of increasing resistance to conventional antifungal agents used in newly clinically isolated strains. Although recombinant cytokines and mono-/poly-clonal antibodies are added into antifungal armamentarium, more effective antimycotic drugs are exceedingly demanded. It is comforting that the development of fungal vaccines and adjuvants opens up a window to brighten the prospective way in the diagnosis, prevention and treatment of fungal assaults. In this review, we focus on the progression of several major fungal vaccines devised for the control of Candida spp., Aspergillus spp., Cryptococcus spp., Coccidioides spp., Paracoccidioides spp., Blastomyces spp., Histoplasma spp., Pneumocystis spp. as well as the adjuvants adopted. We then expound the interaction between fungal vaccines/adjuvants and host innate (macrophages, dendritic cells, neutrophils), humoral (IgG, IgM and IgA) and cellular (Th1, Th2, Th17 and Tc17) immune responses which generally experience immune recognition of pattern recognition receptors, activation of immune cells, and clearance of invaded fungi. Furthermore, we anticipate an in-depth understanding of immunomodulatory properties of univalent and multivalent vaccines against diverse opportunistic fungi, providing helpful information in the design of novel fungal vaccines and adjuvants.

Assessment of hepatitis B virus infection and tuberculosis among people living with HIV at the Kankan Regional Hospital (Republic of Guinea)

Objective: The aim of this study was to determine the tuberculosis and hepatitis B virus co-infection among people living with HIV at the Kankan Regional Hospital (HRK) in Guinea and to describe the biological and clinical signs associated to the co-infections. Methods: It was 4 years retrospective study (January 1st, 2015-December 31st, 2018. data was collected from lab registers and hospitalization files. Results: On a total of 345 PVVH, HBsAg testing was carried out. Thus 9.3% (32/345) were co-infected with HIV/HBV with the presence of jaundice in 8.1% (28/345). All patients (100%) had oropharyngeal candidiasis (thrush). About 44.1% (152/345) of patients tested positive for tuberculosis, while 49.6% (171/345) presented with prurigo. The results of the study showed that the female gender was predominant with a sex ratio (M/F) = 0.69. The average age of the patients was 38.45±13.38 [16-80 years]. The most represented age group was ≥35 years (55.9%), followed by 25-29 years (16.8%) and 30-34 years (14.2%). More than half of the patients were married (51.6%), and singles accounted for 31.0%. On a socio-professional level, workers were in the majority (54.7%), followed by farmers (15.1%) and traders (14.5%). Conclusion: All of these results show that the prevalence of tuberculosis and hepatitis B was high among people living with HIV at the Kankan Regional Hospital.

Oropharyngeal Candidiasis, Candida Albicans Infections, and Oral Immune Mediators Associated with Oral Human Immunodeficiency Virus: A Literature Review

Introduction: While Candida albicans are usually commensal and present in low density in the oral cavity of healthy individuals, an immunocompromised immune system can lead to the overgrowth of this fungal species, leading to oral microbiome “dysbiosis” and activation of immune responses. In severe cases, C. albicans overgrowth can lead to an oral infection called oropharyngeal candidiasis (OPC), which is associated with inflammation, lesions, and sores of the oral cavity. While human immunodeficiency virus (HIV) infection has been linked to an increased risk of OPC, few studies have associated OPC and C. albicans infection with subsequent risk for oral HIV acquisition. Evidence on the oral microbiome and how it can alter HIV risk is also lacking. Methods: A literature search was performed on PubMed, Google Scholar, and the University of Alberta Library Database from inception to November 2023. Results and Discussion: The risk of oral HIV transmission is low. OPC and C. albicans fungal infection can increase HIV susceptibility by activating immune responses associated with the clearance of microbial pathogens, inducing inflammation and elevations in cytokines related to HIV risk including IL-17, IL-6 and IL-1ß. Persistent C. albicans infections also promote the recruitment of T-helper 17 cells, which is a common HIV target cell, and neutrophils, which releases neutrophil proteases upon inflammation and mediates the cleavage of tight junction proteins, ultimately disrupting the oral microbiome. Conclusion: Increased immune cell recruitment to the mucosa and increased epithelial breakdown may facilitate the diffusion and access of HIV virions across the epithelium to immune target cells, suggesting that OPC and C.albicans infections has the potential to increase risk for oral HIV acquisition. Limited evidence of the relationship between C. albicans density, OPC, and oral HIV risk, warrants high-quality cross-sectional studies in the future.

Coptidis rhizoma extract alleviates oropharyngeal candidiasis by gC1qR-EGFR/ERK/c-fos axis-induced endocytosis of oral epithelial cells

Ethnopharmacological relevanceCoptidis rhizoma, first recorded in the “Shen Nong's Herbal Classic”, is one of the traditional Chinese medicine (TCM) used to treat infectious diseases, with reputed effectiveness against oropharyngeal candidiasis (OPC). Studies have demonstrated the inhibitory properties of C. rhizoma (CRE) against Candida albicans, yet there is limited information available regarding its treatment mechanism for OPC. Aim of the studyOur previous research has suggested that CRE can prevent the formation of C. albicans hyphae and their invasion of the oral mucosa, thereby exerting a therapeutic effect on OPC. Nevertheless, the precise therapeutic mechanisms remain incompletely understood. Previous studies have revealed that a receptor for globular heads of C1q (gC1qR), a crucial co-receptor of the epidermal growth factor receptor (EGFR), facilitates the EGFR-mediated internalization of C. albicans. Therefore, this study aims to investigate the potential mechanism of action of CRE and its primary component, berberine (BBR), in treating OPC by exploring their effects on the gC1qR-EGFR co-receptor. Materials and methodsTo identify the chemical components of CRE, we utilized Ultra-high performance liquid chromatography in conjunction with quadrupole time-of-flight mass spectrometry (UPLC-Q/TOF-MSE), revealing the presence of at least 18 distinct components. To observe the therapeutic effects of CRE on OPC at the animal level, we employed hematoxylin and eosin staining, periodic acid-Schiff staining, scanning electron microscopy, and fungal load detection. Subsequently, we evaluated the anti-inflammatory properties of CRE and its main component, BBR, in treating OPC. This was achieved through enzyme-linked immunosorbent assay (ELISA) both at the animal and cellular levels. Additionally, we assessed the ability of C. albicans to disrupt the epithelial barrier of FaDu cells by studying the protective effects of BBR on the fusion barrier using the transwell assay. To further explore the underlying mechanisms, we analyzed the effects of BBR on the gC1qR-EGFR/extracellular signal-regulated kinase/c-Fos signaling pathway at the cellular level using qRT-PCR, western blotting, and immunofluorescence. Furthermore, we validated the effects of BBR on the gC1qR-EGFR co-receptor through ELISA, qRT-PCR, and western blotting. Finally, to confirm the outcomes observed at the cellular level, we validated the impact of CRE on the gC1qR-EGFR co-receptor in vivo using qRT-PCR, western blotting, and immunofluorescence. These comprehensive methods allowed us to gain a deeper understanding of the therapeutic mechanisms of CRE and BBR in treating OPC. ResultsOur findings indicate that CRE and its primary component, BBR, effectively alleviated the symptoms of OPC by modulating the gC1qR-EGFR co-receptor. The chemical composition of CRE and BBR was accurately identified using UPLC-Q/TOF-MSE. The gC1qR-EGFR co-receptor plays a crucial role in regulating downstream signaling pathways, emerging as a potential therapeutic target for OPC treatment. Through both in vitro and in vivo experiments, we explored the therapeutic potential of CRE and BBR in OPC. Additionally, we employed overexpression and silencing techniques to confirm that BBR can indeed influence the gC1qR-EGFR co-receptor and regulate the gC1qR-EGFR/extracellular signal-regulated kinase (ERK)/c-Fos signaling pathway, leading to improved OPC outcomes. Furthermore, the significance of CRE's effect on the gC1qR-EGFR co-receptor was validated in vivo. ConclusionOur study demonstrates that CRE and its main component, BBR, can effectively alleviate OPC symptoms by targeting the gC1qR-EGFR heterodimer receptor. This discovery offers a promising new therapeutic approach for the treatment of OPC.

Fluconazole-Loaded Ibuprofen In Situ Gel-Based Oral Spray for Oropharyngeal Candidiasis Treatment.

Oral candidiasis is a fungal infection affecting the oral mucous membrane, and this research specifically addresses on a localized treatment through fluconazole-loaded ibuprofen in situ gel-based oral spray. The low solubility of ibuprofen is advantageous for forming a gel when exposed to an aqueous phase. The 1% w/w fluconazole-loaded in situ gel oral sprays were developed utilizing various concentrations of ibuprofen in N-methyl pyrrolidone. The prepared solutions underwent evaluation for viscosity, surface tension, contact angle, water tolerance, gel formation, interface interaction, drug permeation, and antimicrobial studies. The higher amount of ibuprofen reduced the surface tension and retarded solvent exchange. The use of 50% ibuprofen as a gelling agent demonstrated prolonged drug permeation for up to 24h. The incorporation of Cremophor EL in the formulations resulted in increased drug permeation and exhibited effective inhibition against Candida albicans, Candida krusei, Candida lusitaniae, and Candida tropicalis. While the Cremophor EL-loaded formulation did not exhibit enhanced antifungal effects on agar media, its ability to facilitate the permeation of fluconazole and ibuprofen suggested potential efficacy in countering Candida invasion in the oral mucosa. Moreover, these formulations demonstrated significant thermal inhibition of protein denaturation in egg albumin, indicating anti-inflammatory properties. Consequently, the fluconazole-loaded ibuprofen in situ gel-based oral spray presents itself as a promising dosage form for oropharyngeal candidiasis treatment.

Correction for Lei et al., “Riboflavin Targets the Cellular Metabolic and Ribosomal Pathways of Candida albicans In Vitro and Exhibits Efficacy against Oropharyngeal Candidiasis”

Correction for Lei et al., “Riboflavin Targets the Cellular Metabolic and Ribosomal Pathways of <i>Candida albicans In Vitro</i> and Exhibits Efficacy against Oropharyngeal Candidiasis”