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Open access peer-reviewed chapter

Effects of Bacterial Biofilm on Immunity in Chronic Tonsillitis

Written By

Fuat Bulut and Aylin Turksever Tetiker

Submitted: 26 January 2025 Reviewed: 14 March 2025 Published: 06 August 2025

DOI: 10.5772/intechopen.1010132

Exploring Bacterial Biofilms IntechOpen
Exploring Bacterial Biofilms Edited by Sadık Dincer, Melis Sumengen Ozdenefe and Hatice Aysun Mercimek Takci

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Exploring Bacterial Biofilms

Sadık Dincer, Melis Sumengen Ozdenefe and Hatice Aysun Mercimek Takci

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Abstract

A great number of children suffer from recurrent tonsillitis attacks in which antimicrobials can only provide temporary relief. Underlying cause of this type of recurrent infections is largely biofilm formation, formed in tonsils. Biofilm development is a major virulent factor behind a vast number of chronic bacterial infections. Once a biofilm is formed, planktonic cells that grow around any tissue can enter a resting phase and begin to generate biofilm matrix. Biofilm is a primitive form of multicellular life and refers to biological systems formed by the functional groups of the bacteria with coordination ability. It is reported that biofilm is not necessarily pathologic on mucosal surfaces. A “healthy” and “pathologic” microbiome has to be present. Pathologic mucosal biofilm can be formed via microorganisms and viruses that are no good for mucosa. Recent studies have verified the connection of pathologic biofilm, on mucosal tissue in particular, with human diseases. In this review, effects of the biofilm in chronic tonsillitis on mucosal immunity, advantages and limitations of mucosal biofilm, chronic diseases emerging in biofilms, and latest treatment options focusing on biofilms have been explored collectively.

Keywords

  • palatine tonsil
  • immunity
  • mucosal
  • bacteria
  • tonsillitis
  • biofilms

1. Introduction

Palatine tonsils has strategic position in oropharynx, upper respiratory tract and gastrointestinal system and plays a major immunological role against the potential infections in these regions [1]. A series of cytokines regulate adhesive molecules in endothelium and epithelium cells; thereby increasing the migration of eosinophils to mucosa. In all these tissues, expression of Toll-like receptors indicates a substantial immunological function of upper airway mucosa [2]. Both humoral and cellular immunological phases are initiated in lymphoid follicles and extra follicles, which exist in crypt epithelium of lymphoids and dendritic cells [3].

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2. Chronic tonsillitis and biofilm

It is safe to claim that in specific forms of tonsillitis, the cause of recurrence and chronicity is bacterial biofilm in the crypt inside infected tonsil. If pathologically, in follicular lymphoid hyperplasia and interfollicular region plasma cell infiltrate to fibrosis or non-fibrosis lymphoid, this phenomenon is named as chronic tonsillitis. Morphological classification of chronic tonsillitis is lymphoid hyperplasia, crypt dilation and parenchymal fibrosis. It is possible to detect heavily calcified structures in crypts. Clinical symptoms can be halitosis, tonsil stones and permanent lymphadenopathies. While the bacteria protect themselves from antibiotics and host defense, they simultaneously secrete endotoxins to the environment. As a result, local endotoxin inside tonsillar crypt leads to chronic inflammation. As is the case in various infections, in chronic tonsillitis too, polysaccharides also known as mucoid extracellular polymers secreted by the bacteria, proteins and teichoic acid are responsible for biofilm formation. Mucosal biofilm hampers the treatment and multiplies the likelihood of complications. Chronic tonsillitis is particularly of great importance because it requires frequent use of antibiotics, develops resistance to antibiotics, causes complications induced by chronic tonsillitis and calls for frequent need for surgical operation. Biofilms can be formed via a single type of microorganism or comprised of more than one type. Bacteria in the biofilm exist embedded into a matrix that acts like mud or slum containing a set of polysaccharide, nucleic acid and protein. They are named as non-cellular polymeric agents. Biofilm matrix may integrate non-cellular mineral crystals, corrosion particles and blood components [4]. Different biofilm architecture determines the exposure of bacteria to phages [5]. The polysaccharides that are synthesized by biofilm microorganisms form the main extracellular component of biofilm. As for the cellular structure of biofilm; 97% consists of water, 2–3% consists of microorganisms, 1% consists of polysaccharide, 1% consists of protein and 1% consists of the DNA and ions. Biofilm development takes place in five stages. Development stages of the biofilm are as shown in Figure 1 [6].

  1. Adhesion of microorganism: Organic and/or inorganic materials adhere to the surface. Next, microorganisms stick to the same surface. This adhesion stage is reversible. In these stages, biofilms are activated by the changes in environmental factors (food concentrations, pH, temperature, oxygen concentration, osmolality and iron)

  2. Irreversible adhesion: In this stage, microorganisms get connected and formed. Those microorganisms are dynamic. Biofilm layer quickly becomes thicker than 10 μm. As signal changes are activated, exopolysaccharide production occurs via genetic mechanisms and planktonic bacteria and food traps also contribute to this compound.

  3. Colonization stage I: Bacteria on the surface form microcolonies

  4. Colonization stage II: Once biofilm thickness exceeds 100 mm, the 4th stage of the colonization, also known as maturation II, occurs. Planktonic bacteria in the environment also attach on these colonies. A few days following this process, the 5th stage emerges.

  5. Detachment: In this stage, cells break up. Certain bacteria that form planktonic phenotype disconnect from the biofilm. A range of bacteria types such as Pseudomonas, Staphylococcus and Haemophilus all have surface adhesion capacity.

Figure 1.

Stages of biofilm development: attachment, proliferation and maturation. Graphics by Peg Dirckx, David Davies and Karin Sauer, courtesy of Dr. Gregory Schultz, WUWHS 2008, Toronto [6].

Once the microorganism adheres to the surface, it then secretes complex polysaccharides that thus embed the bacteria. These micro-colonies gradually expand and named as “Quorum sensing” to refer to a large and wide form of settled bacteria. These are resistant toward treatment with various mechanisms implemented via planktonic bacteria [7]. Biofilm becomes infectious the moment it is formed. After the bacteria adhere to a surface and form the biofilm, they can no longer be detached from the surface via gentle rinsing [8].

Additionally, although microorganisms settled in biofilm are quite sensitive toward antimicrobials in culture plates under planktonic conditions, under high concentrations, they can survive even under the presence of bacteria killing antimicrobials [9]. Microbial biofilms are visible in more than 65–80% of all human bacterial infections [10]. The significance of biofilm among recurrent tonsillitis and peritonsillar abscess patients has been put forth [11]. Studies have reported the capacity to form biofilm in tonsil tissues of chronic tonsillitis patients [12]. Bacterial biofilm has been detected in saliva stones in mouth [13].

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3. Effects of biofilm on mucosal immunity

A recent study has revealed the role of biofilms in immunity [14]. Bacterial biofilms in mouth suppress β6 integrin by weakening TGF-β1 signaling, which then leads to a developed pro-inflammatory response [15]. There is connection between bacterial infections and autoimmunity [16]. As a response to aggressive periodontitis treatment, the gravity of local IL-10 level has been demonstrated [17]. Mouth bacteria secrete pro-inflammatory cytokines, and through inflammation, it affects systemic diseases [18]. Inborn immunity plays role in the development of biofilm in pediatric respiratory infections [19]. Stress hormones have effects on microbial infections [20]. Pro-inflammatory cytokine IL-1β strongly increases biofilm formation [21]. S. epidermidis biofilms, immune-activating cytokines and TNFα elevate the expression of IL-6, IL-10, IL-1β and IFNγ [22, 23]. It has been acknowledged that biofilm plays direct role in pathogenesis. In chronic mucosal inflammation, self-antigens or allergens enable the formation of biofilm as a response. Local inflammation cytokines or excess mucus can also back up biofilm development [24]. It has been argued that some other factors also render the potential effect in mucosal biofilm pathogenesis. These include mucus compound and liquid flow, specific inborn epithelium defense mechanisms and epithelium’s capacity to synthesize the antimicrobial molecules. In order to grasp mucosal role of the biofilm, it is vital to clearly manifest its host response against biofilm in chronic diseases.

In most of the chronic diseases, the role of biofilm is generally indirect. The context of regional lesions or tissue damage depends on the contribution of virulent factors specific to the disease inducting mucosal biofilm. In order to fully understand the pathogenesis of mucosal biofilms, it is quite important to conduct a local analysis of tissue virulence and the stage of biofilm. It has been reported that P. aeruginosa, Staphylococcus aureus, Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis and many other mucosal pathogens can form biofilm. The bacteria sticking to tonsillar epithelium particularly stay within tonsillary crypt and can become a mixed colony of the bacteria. While the bacteria protect themselves from the antibiotics and host defense, they simultaneously release their endotoxins to the environment. Biofilm’s mixed microorganisms and virulence factors result in tissue damage. In human diseases, the role of mucosal biofilm can best be defined through the two pathogenesis models of host inflammatory response. Biofilm’s mixed microorganisms and virulence factors result in tissue damage. In diseases, the role of mucosal biofilm can best be defined through the two pathogenesis models of host inflammatory response. In the first model, mucosal biofilms indirectly starts excessive pro-inflammatory response [25]. In the second model, on the other hand, biofilm components such as extracellular matrix can lower mucosal inflammatory response of the infection and develop phagocytic cell function disorder [26]. This phenomenon offers an advantage in the early development of biofilm organisms. Similar to mucosal tissue, host receptor microbial adhesion system also contributes to the feeding environment of biofilm organisms. In the biofilm that is formed via Streptococcus pyogenes in tissue and abiotic surfaces, there is approximately 50% variance in gene expression [27]. Extracellular matrix of the biofilm leads to antibiotic resistance upon secreting polymers that bind and deactivate the antimicrobials [28]. Compared to their planktonic counterparts, microorganisms in biofilms can be 500–1.000 times more tolerant toward antibacterial components [29]. In chronic mucosal inflammations self-antigens or allergens allow the formation of biofilm as a response. Locally inflammatory cytokines or excessive mucus can also contribute to biofilm formation [24]. In mucosal biofilm, there is biofilm formation associated with adaptive T and B cells in which innate immune response is due to tissue destruction by plenty of neutrophils and macrophages, matrix metallo proteinases and reactive oxygen species (ROS) and inflammatory cytokines (IL-1, PGE2, TNF-a, IL-1b) [30]. Host response contributes to the improvement of oral biofilm through collecting pro-inflammatory cells (neutrophils and macrophages), secretion of inflammatory mediator (interleukin-1 [IL-1] and prostaglandin E2) and matrix metallo proteinases (MMPs) [31] In inflammation, firstly, by releasing ROS to which neutrophils are hypersensitive in periodontal diseases, they contribute to disease progress which in turn damage proteinases, host gum and periodontal ligaments [32]. Neutrophils promote proinflammatory cytokines such as leukotriene B4, IL-6, tumor necrosis factor-a (TNF-a) and IL-1b [33]. Between biofilm and human immune system, a number of complex and multidimensional interactions, which alter host environment, condition biofilm phenotype and affect the functionality of host immune cells emerge [34]. Biofilms induce apoptotic process [35]. In a previous study we conducted, we exhibited the similarity between clinical picture of pediatric patients whose both mother and father have chronic tonsillitis and periodic fever, aphthous stomatitis, pharyngitis, adenitis (PFPA syndrome) [36]. On the other hand, it has been detected that bacterial biofilms substantiate the conditions that lead to oncogenic transformation of epithelium cells [37]. In otolaryngology, a review on biofilms and pathogenesis, diagnosis and treatment strategies has been conducted Figure 2 [38].

Figure 2.

Biofilms in ENT: understanding the pathogenesis, diagnosis and treatment. GhoshMoulic et al. [38].

Tonsil surface swab bacterial culture results are different from tonsil core in recurrent tonsillitis [39]. It demonstrates ex vivo the quantity and spatial distribution of gram-positive biofilms in multimodal optic mesoscopy tonsillary [40]. A number of studies focusing on increasing the biological significance of biofilm models have been reported [41]. Studies have been conducted to expedite the emergence productive biofilms in biology-based production stages [42]. Although in chronic tonsillitis we have clinically observed the effects of bacterial mucosal biofilms on immunological figures there is still need for biochemical, genetic and molecular studies in this field.

3.1 Beneficial biofilms

In animal models of biofilm, it has been demonstrated that in oral mucosa cancer treated with tretinoin, biofilm proves to be of use in the prevention or limitation of the tumor [43]. Biofilms are effective in the treatment of industrial wastes and removal of nitrogen and phosphorus [44]. They are, as studies show, effective in increasing bioelectric production [45]. Studies have documented the relationship between bacterial biofilms and immuno-modulation specific to anatomical site [46]. They are used in waste water treatment [47]. Biofilms can greatly diminish necrotizing enterocolitis incidence and its frequency [48]. Biofilms are a membrane system resistant to contamination [49]. Beneficial oral biofilms are used as smart bioactive interfaces [50]. Studies have reported specific biofilms that can be useful for tomato roots [51].

3.2 The near future of biofilm

In otorhinolarynologist infections, biofilm-induced infections have gained more popularity each new year. In a previous study we conducted, we have put forth the thickness and significance of bacterial biofilm in children with chronic tonsillitis whose mother and father both have chronic tonsillitis as shown in Figure 3 [52].

Figure 3.

Mucosal biofilm in tonsil tissue of children with a history of recurrent/chronic tonsillitis [52].

Some studies have pointed at the relationship between cancer and bacterial biofilm [53]. As is the case in most of the chronic contagious diseases, biofilm-induced infections are also usually asymptomatic in early stages of chronic tonsillitis. When host defense is low, planktonic or free-living microorganisms can disintegrate from biofilm when host resistance is weak and can cause acute infection. Microbial biofilms significantly impact human health by rising morbidity, mortality and health care costs. The importance of anti-biofilm treatments in sleep disorders and recurrent chronic tonsillitis has been detected [54]. It has been reported that ROS impedes biofilm formation [55]. Biofilm morphology has been designed for high sensitivity of bioelectrochemical sensor [56]. Studies have exhibited the role of biofilm distribution-based nanoparticles in the prevention of re-infection [57]. Besides, it has been reported that local anesthetics create antimicrobial impact [58]. As an alternative treatment ultrasound can efficiently kill the bacteria via cavitation and peroxide production inside or onto bacteria cells and thus can increase the efficiency of antibiotic treatment [59]. Nanoparticles have been suggested for oral biofilm treatments [60]. It has been reported that mechanically induced saliva has impact on the oral biofilm formation [61]. Magnesium has been detected to exhibit antimicrobial effects [62]. Microrobots are suggested to have effects on oral biofilms [63].

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4. Conclusion

In recent years, studies related to mucosal biofilms in otorhinolarynology have gained impetus. Emerging pathological mucosal biofilms are the main cause of resistance toward medical treatment and render negative effects on mucosal immunity. Mucosal biofilms are the primary reason of recurrent tonsillitis in both pediatric and adult patients. Upon the development of experimental models in biofilm-induced infections, therapeutic strategies that can be effective on biofilm can also be developed. By this way, potential complications likely to occur in many types of chronic infections can be diminished. Drug therapies in chronic infectious diseases can be modeled by prioritizing the biofilm. Hence, different drug combinations according to experimental models can be developed. In near future, more detailed and comprehensive studies will shed light on the effects of bacterial biofilms on mucosal immunity of patients with chronic tonsillitis.

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Conflict of interest

No potential conflict of interest relevant to this article was reported.

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Written By

Fuat Bulut and Aylin Turksever Tetiker

Submitted: 26 January 2025 Reviewed: 14 March 2025 Published: 06 August 2025

© 2025 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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