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Department of Pharmaceutics, Karnataka College of pharmacy
Tonsillitis is a common upper respiratory infection that affects the palatine tonsils; it results from Streptococcus pyogenes. Although oral formulation of macrolides Azithromycin/ Clarithromycin is generally recognized as a treatment for tonsillitis, it presents limitations such as the low aqueous solubility of the drugs in the mouth. Moreover, the bitter taste of these drugs results in pediatric non- adherence. The use of the intranasal route provides an attractive option for the treatment of tonsillitis as it exhibits a large absorption surface area, allowing faster absorption of the drug into the lymphatic system. The main goal of this research study is to develop and evaluate a neosomal in-situ gel system for intranasal delivery of a macrolide antibiotic by combining the advantages of niosomes, vesicular carriers that enhance the solubility and permeation of drugs, with in-situ gelling technology, which prolongs nasal residence time. Niosomes enhance tonsillitis treatment by improving the solubility and stability of macrolides. Their small size and lipid nature facilitate deeper mucosal penetration into lymphatic tissues, while their ability to provide sustained drug release reduces dosing frequency, masking the bitter taste of antibiotics and significantly improving patient compliance. Some challenges in preparing niosomes for treatment of tonsillitis may involve preventing aggregation or drug leakage during storage. Furthermore, the surfactant-to-cholesterol ratio plays a significant role in preventing drug leakage, although mucociliary clearance rate in the nasal route used may require special gelling properties to optimize drug exposure time. The next course of research that can be taken up is human trials for safety and the analysis of “smart” gels that respond specifically to the presence of an infection. Improving the design of nasal sprays for better dosing and how these gels can target the lymphatic system will make treatment an even bigger success.
Tonsillitis is defined as an inflammatory condition affecting the palatine tonsils which may be secondary to virus or bacteria infection and can be considered one of the leading causes of throat pain seen in primary practice[1]. Palatine tonsils are part of Waldeyer's ring and are vital in maintaining mucosal immunity as they act as the first line of defense in inhalation and ingestion of pathogens[2]. Viral infections are more prevalent than bacterial infections as causative factors in acute tonsillitis, while Group A β-hemolytic Streptococcus is the most common cause of tonsillitis in which antibiotics must be used [3]. Classic presentation includes throat pain, fever, difficulty swallowing, redness and exudates of the tonsils, and painful cervical lymphadenopathy[4]. Prompt diagnosis and appropriate management are essential to prevent complications, minimize unnecessary antibiotic use, and improve patient outcomes[5].
Figure 1: Tonsillitis
1.1 Types of Tonsillitis
1.2 Introduction of Bio-film
Biofilm is a well-structured cluster of microorganisms attached to the surface of biotic or abiotic objects and enveloped in an extracellular polymeric substance (EPS) layer produced by themselves, which acts as a barrier against environmental stress for microbial cells[9]. The process of biofilm development involves several consecutive phases, such as primary adhesion, irreversible attachment, microcolony formation, maturation, and dispersion, providing microorganisms with a chance to live in unfavorable environments[10]. Biofilm formation plays a significant role in causing chronic diseases due to the ability of the EPS layer and the changed physiology of bacteria to provide resistance to both antibiotics and the immune system of the host[11].
1.2.1 Formation of Bio-film[12]
Figure 2: Biofilm formation
1.3 Pathophysiology of recurrent acute tonsillitis
Palatine tonsils are paired lymphoid glands that reside in the oropharynx and are considered parts of Waldeyer’s ring, along with adenoids, lingual tonsils, and tubal tonsils. These act as the body's first defense mechanism against pathogens that enter via the mouth. Inflammation and injury to the tissues occur when microorganisms surpass this mechanism. This condition is called tonsillitis.[13]
1.3.1 Entry of Pathogens and Colonization
Pathogenesis starts with infection by microorganisms via the epithelial crypts of the palatine tonsils. The crypts being deep offer a lot of surface area, which is good for antigen sampling but also offers a good habitat for microbes to thrive in.
The most common causative organisms include:
1.3.2 Activation of Innate Immune Response
Once they cross the lining epithelium of the tonsils, these pathogens are identified through pattern recognition receptors (PRRs), especially Toll-like receptors (TLRs) present in the epithelium, dendritic cells, macrophages, and neutrophils.
The identification of these pathogen-associated molecular patterns (PAMPs) initiates the process of activating various intracellular signaling pathways, like the one for NF-κB, which results in the secretion of several inflammatory mediators like:
These mediators increase vascular permeability, vasodilation, and leukocyte recruitment, producing the characteristic inflammatory signs[15]
1.3.3 Inflammatory Cell Recruitment
Inflammation leads to the secretion of chemokines, which help in attracting:
Neutrophils phagocytize bacteria and secrete reactive oxygen intermediates and proteases. While these help in eliminating the microorganisms, these cause injury to the surrounding tissues of tonsil leading to erythema, edema, and purulent exudate.[16]
1.3.4 Adaptive Immune Response
There are numerous B and T lymphocyte follicles within the palatine tonsils.
After presentation of antigens:
This adaptive immunity system is responsible for elimination of pathogens and memory generation. Nevertheless, in case of severe infection, tonsils enlargement occurs due to lymphoid hyperplasia.[17]
1.3.5 Tissue Changes During Acute Tonsillitis
The features of acute inflammation include:
These pathological changes lead to the clinical manifestations that include:
1.3.6 Mechanism of Pain
Pain in tonsillitis is caused by inflammation of the mediators that sensitize nociceptors present in the mucous membrane of tonsils.
Some major pain mediators include:
These pain mediators act on TRP channels, especially TRPV1 receptors, causing a lower pain threshold and giving rise to painful sensation in the throat[19]
1.3.7 Chronic Inflammation
Repeated infections result in:
These changes impair normal tonsillar immune function, making recurrent infections more likely[20].
1.3.8 Potential Complications
When infection persists without treatment:
These complications are caused by bacterial invasion or immune[21]
1.4 Aetiology of Tonsillitis
Tonsillitis is an inflammatory condition that affects the palatine tonsils, and its common cause is infection by either viruses or bacteria. Palatine tonsils make up the Waldeyer's ring, and this ring acts as the first immunological defense mechanism in the body to protect from pathogens inhaled or ingested. When infection takes place, it happens due to pathogenic agents that overwhelm the local immune system, multiply in the crypts of tonsils and cause inflammation. Viruses are the cause of 70-95% of tonsillitis cases[22].
1.4.1 Viral Aetiology
Tonsillitis is mostly caused by viruses, particularly in children under the age of five years. These infections are often self-limiting in nature, and they occur alongside other upper respiratory tract infections.
The aforementioned viruses infect the epithelium of tonsils, which causes tissue damage and activation of the immune system, resulting in tonsillitis and sore throat. Tonsillitis caused by viruses is usually self-limiting within 5-7 days[23].
1.4.2 Bacterial Aetiology
Between 5% and 30% of tonsillitis may be due to bacterial infections, based on age groups. Bacterial tonsillitis is significant from a clinical point of view because of the presence of complications, both suppurative and non-suppurative.
Streptococcus pyogenes (Group A β-hemolytic Streptococcus, GAS)
Streptococcus pyogenes is the most common bacterium responsible for tonsillitis. It attaches itself to tonsil surface cells using M proteins and adhesins, produces toxins and causes inflammation.
1.4.3 Mixed (Polymicrobial) Infection
Other patients may have mixed viral and bacterial infections where the upper respiratory viral infection causes damage to the tonsillar epithelium and renders the area susceptible to bacteria.
Examples include:
Mixed infections have been found to cause prolonged illness[25].
2. Mode of Transmission
Tonsillitis refers to a communicable infection of the palatine tonsils which is brought about by either viral or bacterial infections. Tonsillitis on its own is not a transmittable disease; however, the microbes that cause the infection may be passed from one individual to another. Modes of transmission include inhalation of airborne microorganisms in the form of respiratory droplets, direct contact with the infectious fluids and indirect contact via fomites[26].
2.1Transmission through Respiratory Droplets
The mode of transmission that occurs most frequently is through respiratory droplets released when an infected individual:
These droplets may include infectious viruses or bacteria, for example, Streptococcus pyogenes. The droplets are inhaled into the lungs or stick to the mucus membranes of the nasal passage, mouth, or throat of another individual close to the infected person. Proximity (about 1 to 2 meters away) is a key factor in the transmission of these diseases. Rhinoviruses, adenoviruses, influenza viruses, coronavirus, and GAS are transmitted mostly by this method[27].
2.2 Direct Person-to-Person Contact
Transmission also takes place through physical contact with infected saliva or respiratory secretions.
Some examples are:
The pathogen enters the body through the mouth or nose via contact with infected secretions and then infects the tonsillar crypts. Children are more vulnerable to the disease because of close interpersonal contacts through play and schooling[28].
2.3 Airborne Spread
Some viruses that cause tonsillitis can be transmitted through aerosols in certain situations, such as poor ventilation indoors, where certain respiratory viruses, including influenza virus and certain types of coronavirus, are found. Nevertheless, for most cases of tonsillitis, the transmission occurs through droplets, while air is less significant for the disease's transmission[29].
2.4 Factors Influencing Transmission
There are many variables that can influence the transmission of pathogens causing tonsillitis:
3. Commonly prescribed drug classes in acute tonsillitis[31]
Figure 3: Commonly prescribed drug classes in acute tonsillitis.
3.1 Mechanism of action of drugs for Tonsillitis treatment
Tonsillitis may be the result of a viral pathogen or Group A β-hemolytic Streptococcus (GAS), with treatments aimed at bacterial infection elimination, alleviation of inflammation and symptomatic management of patients, as well as complications prevention[32]. β-Lactam antibiotics (penicillin and amoxicillin) act as bactericidal agents due to the interaction with PBPs leading to the inhibition of cell wall synthesis and destruction of bacteria[33]. Macrolides (azithromycin, clarithromycin, and roxithromycin) inhibit bacterial protein synthesis via binding with the 50S ribosomal subunit, blocking peptide chain formation[34].
Non-steroidal anti-inflammatory drugs (NSAIDs) decrease pain, fever and inflammation due to COX enzymes inhibition and, thus, suppression of prostaglandins production [35].
Paracetamol (acetaminophen) is an analgesic and antipyretic agent, which works by central inhibition of prostaglandins synthesis [36]. Corticosteroids (mainly dexamethasone) help to lower inflammation and tonsillar edema by inhibition of inflammatory cytokines and fasten the process of symptoms' reduction as add-on therapy[37].
4. Clinical Practice[38]
|
Clinical recommendation |
Evidence rating |
comments |
|
In the primary care setting, a clinical scoring system such as the centor score can be applied when examining patients with symptoms of pharyngitis and/or tonsillitis; rapid antigen detection testing should also be considered in patients with a score of 2 or more. |
A |
Meta-analysis and validated clinical decision rule |
|
Antibiotics are indicated for group A beta-hemolytic streptococcus pharyngitis and Penicillin is the drug of choice. |
A |
Infectious diseases society of America clinical guidelines and meta-analysis |
|
When considering recurrent tonsillitis, the preferred option over tonsillectomy in case of watchful waiting, in the presence of fewer than 7 attacks in the previous year, fewer than 5 per year in the previous 2 years, or fewer than 3 per year in the previous 3 years, respectively. |
A |
Systematic review and clinical practice guideline |
A = consistent, good quality patient-oriented evidence; B = inconsistent or limited quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion or case series.
5. Patent for Lactic Acid Tonsillitis Treatment
One of the oldest patents that specifically pertains to tonsillitis is the patent for a treatment that contains lactic acid and which can be used for tonsillitis, pharyngitis, and any other throat infection.
Important attributes :
Importance :
The above patent provided a novel idea of administering anti-microbial action through local means rather than the traditional use of systemic antibiotics, and it was still considered important between 2010 and 2025[39].
6. Antibiotic Dosages and Marketed formulations available[40]
Table 1: Antibiotic dosages for adults and children with Group A beta-hemolytic streptococcal tonsillitis
|
Antibiotic |
Adult Dosage |
Child Dosage |
Duration |
|
Penicillin V |
500 mg two to three times daily |
≤27 kg: 250 mg two to three times daily >27 kg: 500 mg two to three times daily |
10 days |
|
Amoxicillin |
250 mg four times daily OR 500 mg twice daily OR 1,000 mg daily OR 775 mg ER (Moxatag) once daily |
50 mg/kg once daily (max 1,000 mg) |
10 days |
|
Penicillin G benzathine (Bicillin L‑A) |
1.2 million units intramuscularly |
≤27 kg: 600,000 units IM |
One injection |
|
Cephalexin |
500 mg twice daily |
40 mg/kg/day in two divided doses (max 500 mg) |
10 days |
|
Cefadroxil |
1,000 mg daily |
30 mg/kg once or twice daily (max 1,000 mg) |
10 days |
|
Cefpodoxime |
100 mg twice daily |
5 mg/kg/dose twice daily (max 100 mg) |
5–10 days |
|
Cefdinir |
300 mg twice daily OR 600 mg daily |
7 mg/kg/dose twice daily OR 14 mg/kg once daily (max 600 mg) |
5–10 days (300 mg) |
|
Azithromycin (Zithromax) |
12 mg/kg/day (max 500 mg) |
12 mg/kg/day (max 500 mg) |
5 days |
|
Clarithromycin |
250 mg twice daily |
7.5 mg/kg/dose twice daily (max 250 mg) |
10 days |
|
Clindamycin (Cleocin) |
300 mg three times daily |
7 mg/kg/dose three times daily (max 300 mg) |
10 days |
7. Nasal Anatomy and Physiology
Nasal medicine delivery is effective owing to the permeability and high vascularisation of the nasal mucosa, which results in rapid absorption and action. This route bypasses first-pass metabolism, enhances bioavailability. Olfactory pathway-directed drug therapy is useful for drugs with poor oral absorption and CNS-targeted treatments. The nasal cavity in adults measures 12-14 cm from the vestibule to the nasopharynx, with a surface area of 150 cm² and volume of 15 ml. The viscosity of nasal secretions effects mucociliary clearance and drug penetration. Adequate physicochemical properties are required for a medication to be soluble in nasal secretions, ensuring proper dissolution and penetration.
The nasal region is separated as several areas including the vestibule, inferior turbinate, middle turbinate, superior turbinate, olfactory region, frontal sinus, sphenoidal sinus, and ethmoid bone's cribriform plate[41]. NALT (Nasal associated lymphoid tissue) is found in the nasal region and Nasopharynx. It has hairs and a coating of mucus that collect germs and debris that are breathed. The nasal structures also carry out vital tasks such immune responses, mucociliary clearance, and
endogenous material metabolism. The middle septum divides the nasal region into two symmetrical halves, each of which extends posteriorly to the nasopharynx and opens at the face through the nostrils[42]. The nasal vestibule, atrium, respiratory region, and olfactory region are the four separate regions that make up each half Anatomy of the Human Nasal Cavity and Upper Respiratory Tract.
Figure 4: Anatomy of the Human Nasal Cavity and Upper Respiratory Tract
8. Factors Affecting Nasal Drug Absorption
Nasal drug absorption is modulated by several physiological, physicochemical, formulation-related, and environmental factors. Physiological factors include blood flow, surface area, and mucociliary clearance, which can rapidly remove the drug from the absorption site. The integrity of the nasal mucosa, such as inflammation, infection, or damage, can significantly alter permeability and absorption[43]. Enzymatic function present in the respiratory epithelium may also lead to metabolic degradation of certain drugs, especially peptides and proteins, thereby reducing their bioavailability. Physicochemical characteristics of the drug, including mol. wt, hydrophobicity, ionisation (pKa), and solubility, play a crucial role; small, lipophilic, and unionised molecules are generally absorbed more efficiently than large, hydrophilic ones. Formulation factors such as pH, tonicity, viscosity, drug concentration, and use of absorption enhancers or mucoadhesive agents can modify drug residence time and permeability across the nasal membrane[44]. Additionally, dosage form and delivery device affect deposition pattern and absorption efficiency and factors affecting nasal drug absorption. Environmental and patient-related factors, including nasal airflow, posture, smoking, age, and pathological conditions like rhinitis, can further influence the extent and rate of nasal drug absorption[45].
Figure 5: Factors Affecting Nasal Drug Absorption
9. Mechanism of Niosomal Tonsil Targeting
Niosomes are nanovehicles based on non-ionic surfactants and have the ability to carry both hydrophilic and lipophilic drugs inside their structures. Although at present, there are no niosomal preparations that use active targeting with the help of ligands for specific targeting of the tonsils, the niosomes can be used for passive tonsil targeting due to the increased accumulation of drug on the tonsillar mucosa, tonsillar crypt penetration, improved internalization by immune cells, and slow drug release[46].
9.1 Mucoadhesion and Prolonged Residence Time
After the application via either intranasal or oropharyngeal routes, niosomes come into contact with the layer of mucus lining the epithelium of the tonsils. The small size and lipid bilayers allow them to get in closer contact with the mucosal membrane, especially when contained in mucoadhesive in-situ gels.
Mechanism :
Advantages :
The above mechanism will be particularly useful with drugs like roxithromycin with low oral bioavailability[47].
10. Novel approaches for Tonsillitis treatment
10.1 Liposomes :
Figure 6: Liposomes
Liposomes are spherical vesicular systems of lipid bilayers that can encapsulate both hydrophilic and hydrophobic compounds, thereby showing their versatile nature as drug delivery systems. They vary from 20 nanometers to several micrometers in diameter. Mostly consists phospholipid bilayer similar to a cell membrane. The characteristics of liposomes have attracted the attention of researchers in the pharmaceutical and biomedical fields, especially in targeting therapeutic agents for cancer treatment.[48]
10.2 Niosomes
Figure 7: Niosomes
Niosomes are uncharged in their structure and consist of a non-ionic surfactant, cholesterol and sometimes charged molecules (ionic amphiphiles). Both hydrophilic and hydrophobic drugs can be entrapped in niosomes, whether in their core or bilayer droplet. Non-ionic surfactants, as the niosomes’ primary constituent, are amphiphilic compounds with polar head groups and non-polar chains. They are more stable, biocompatible and less toxic.[49]
10.3 Hydrogels :
Figure 8: Hydrogels
Hydrogels are classified on the basis of their components into naturally derived hydrogels, synthetic hydrogels, or a combination of both. These hydrogels are versatile polymeric preparations employed in the application of drugs. The cross-link polymer chains in hydrogels enable them to hold high amounts of aqueous preparations. These are highly stable, fully responsive to outside stimuli, highly loaded, biocompatible, biodegradable, and super absorbable.[50]
10.4 S.L.N (Solid Lipid Nanoparticles)
Figure 9: Solid Lipid Nanoparticles
SLNs have shown promising development and progress in enhancing bioavailability, biodistribution, and therapeutic efficacy of pharmaceutically problematic compounds. They are colloidal carriers combining the advantages of polymeric nanoparticles, emulsions, and liposomes. SLNs embodies the key advantages like excellent biocompatibility, high drug loading capability, controlled release, biodegradability, enhanced pharmacokinetic profile, physical stability, and scalability.
Characteristic features of SLNs, such as drug payload efficacy, physical stability, and release behavior, are controlled by crystallinity and polymorphic behavior of the lipid. Despite initial claims, changes taking place within the crystallinity level and polymorphic behavior of lipids on storage introduce physical instability in SLNs system and the loss of their characteristic features. Lipids such as fatty acids build highly cross-linked particles with a perfect crystal lattice with low drug load.[51]
11. Methods of preparation of nanocarriers
11.1 Thin film hydration:
Figure 10: Thin film hydration
The thin film hydration method involves dissolving the lipid and its related lipophilic drug in a volatile organic solvent, such as chloroform or methanol. After dissolving the lipid, the volatile organic solvent is removed using evaporation under reduced pressure via a rotary evaporator, and this results in a thin film of phospholipid that is attached to the side of the container. In addition, the addition of the aqueous medium in saline or in buffer in the container hydrates the lipid film. This procedure follows hydration in achieving the self-assembly of lipids in vesicles, hence the creation of liposomes. Additionally, sonication of the lipids in the aqueous medium in the container leads to formation of MLVs and MVVs.[52]
11.2 Reverse Phase Evaporation :
Figure 11: Reverse phase evaporation
The emulsion can be developed by compounding a liquid dispersion consisting of an aqueous phase-containing medicinal with a lipid solution in an organic solvent via reverse phase evaporation method. Additionally, this mixing machine is exposed to controlled evaporation of the solvent to form liposomes/Niosomes. This means as the solvent evaporates, it leads to coalescence around the aqueous phase and then finally liposomes/ Niosomes.[53]
11.3 Sonication :
Figure 12: Sonication
This method involves applying ultrasonic energy to the suspension of liposomes/ Niosomes, breaking MLVs into SUVs. Probe sonication delivers energy directly, but bath sonication does it in a controlled manner. However, sonication has low encapsulation efficiency and may damage the sensitive components of liposomes/ Niosomes.[54]
10.4 Ether injection method :
Figure 13: Ether injection method
Slow intravenous injection of surfactant; Cholesterol (150 micro mol) is introduced into 20 ml of ether through a 14-gauze needle (25 ml/min.) in an already heated 4 ml water phase maintained at 60°C.
The ether solution was evaporated in a rotary evaporator, forming a single layered vesicles after evaporation of the organic solvent.SUVs and LUVs prepared by the solvent injection method have a large entrapped aqueous volume.The final vesicle diameter ranges from 50nm to 1000nm.[55]
11. In-Situ Gel Drug Delivery System
In situ gel can be defined as a stimuli-sensitive drug delivery system in which drugs are delivered through a low viscosity liquid (sol) form, which transforms into a three-dimensional polymeric matrix upon exposure to stimuli like body temperature or pH. This system increases the residence time of the drug, offers sustained drug release, increases bioavailability, and ensures better patient compliance. In-situ gels have been used in the delivery of drugs through ocular, nasal, oral, buccal, gastrointestinal, vaginal, rectal, and injectable routes, with more attention towards intranasal route because of reduced mucociliary clearance and increased absorption of drug at the target site[56].
11.1 Types of In-Situ Gel Systems
11.1.1 Temperature-Triggered In-Situ Gel
11.1.2 pH-Triggered In-Situ Gel
11.1.3 Ion-Activated In-Situ Gel
Gelation is the process through which polymers react with physiological ions, namely:
Common Polymers
11.2 Polymers Commonly Used[60]
Table 2: Commonly used polymers
|
Polymer |
Gelation mechanism |
Application |
|
Poloxamer 407 |
Temperature |
Nasal, ocular, injectable |
|
Poloxamer 188 |
Temperature |
Nasal formulations |
|
Carbopol 934/940 |
pH |
Nasal, oral, ophthalmic |
|
Gellan gum |
Ionic |
Nasal, ocular |
|
Sodium alginate |
Ionic |
Oral, nasal |
|
Pectin |
Ionic |
Oral, nasal |
|
Chitosan |
pH/ Mucoadhesive |
Nasal, buccal |
|
HPMC |
Viscosity enhancer |
In-situ gel formulations |
11.3 Application of In-situ gel in Tonsillitis Treatment
The treatment of tonsillitis with intranasal or oropharyngeal in-situ gels has certain benefits:
The use of niosomes with in-situ gels offers two-fold benefits, with niosomes being used for better encapsulation and controlled delivery of the drug and in-situ gel serving to increase the dwell time of the drug[61].
11.4 Advantages of Niosomal Loaded In-Situ Gel
Some advantages that in-situ gels have over traditional preparations include:
11.5 Evaluation Parameters of In-situ gel
Parameters to be assessed in case of niosomal in-situ gel include:
12. Curcumin :
One of the main active components of turmeric extract is curcumin, which comes from Curcuma longa, a type of herb that belongs to the ginger family and is widely grown in tropical regions of southern and southwest Asia. Typically, curcumin is added to food or cooking as a coloring agent. It has been demonstrated that curcumin has direct, broad-spectrum antibacterial properties against both Gram-positive and Gram-negative bacteria. Additionally, curcumin functions as an immunomodulator, improving host-mediated immunity and preventing the pathogen's virulence factors to lessen bacterial infections. Curcumin exhibits significant synergistic or additive antibacterial activity when combined with some conventional antibacterial medications, making it a promising broad-spectrum antibacterial adjuvant to permeabilize the bacterial membrane.[64]
12.1 Antibacterial activity of Curcumin
Figure 14: Antibacterial activity of Curcumin
Curcumin, a primary component of Curcuma longa, is an excellent broad-spectrum antibacterial agent against both Gram-positive and Gram-negative bacteria including S. aureus, MRSA, E. coli, and P. aeruginosa. Curcumin prevents the growth of bacteria via interfering with cell wall stability, preventing FtsZ protein, which is involved in cell division; inhibiting quorum sensing and biofilm formation in bacteria, as well as ROS-mediated injury to bacteria.
The antibiotic potential of curcumin is further improved via its synergistic action. While low solubility in water impedes its application in therapies, nano-formulations such as niosomes substantially increase the stability and efficiency of curcumin[65].
12.2 Curcumin and Macrolide Antibiotic-Loaded Niosomal In-situ Gel Formulation
The novel drug delivery system of a curcumin and macrolide antibiotics loaded niosomal in-situ gel is a highly sophisticated localized drug delivery system meant for the effective treatment of tonsillitis and other URTIs. Here, the combination of curcumin and macrolide antibiotics like roxithromycin or azithromycin are enclosed in niosomes that are suspended in the in-situ gelling polymeric solution. On application to the mucosal membrane (like the nasal or oral mucosa), the solution gets converted into gel form due to changes in certain physiological factors such as temperature, pH, or ionic strength.
REFERENCES
Anik Biswas, Rashmi Mathews, Beny Baby, A Review on Niosomal Insitu Gel Formulations for Intranasal Delivery of Macrolide antabiotics for treatment of Tonsillitis, Int. J. of Pharm. Sci., 2026, Vol 4, Issue 9, 2283-2304. https://doi.org/10.5281/zenodo.22846970
10.5281/zenodo.22846970