Apoptosis in chronic tonsillitis and tonsillar hypertrophy

Önal, Merih; Yılmaz, Taner; Bilgiç, Elif; Müftüoğlu, Sevda; Kuşçu, Oğuz; Günaydın, Rıza Önder

doi:10.1016/j.ijporl.2014.12.005

Cited by 23 publications

(27 citation statements)

References 25 publications

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“…Reduced numbers of follicles and fibrosis in extrafollicular tissue with a strong inflammatory process characterise recurrent tonsillitis . Lymphocytes are higher proliferative, promoting adenotonsillar hyperplasia more often in the tonsils of children with OSA than in the tonsils of children with recurrent tonsillitis . Recently, significant differences have been shown in bacterial community composition and local lymphocytic responses to bacterial microcolonies within the tonsil crypts according the pathologic process.…”

Section: Discussionmentioning

confidence: 99%

Impact of adenotonsillectomy on the evolution of inflammatory markers

Marcano-Acuña

Carrasco-Llatas

Tortajada‐Girbés

et al. 2019

Clinical Otolaryngology

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Background Tonsils are first‐line host defence organs against pathogenic agents and participate in local and systemic immunity. Persistent increases in systemic inflammatory responses may contribute to associated morbidity. The aim of this study was to verify the short‐ and long‐term impact of adenotonsillectomy on the evolution of inflammatory markers in 3‐ to 9‐year‐old children. Methods A prospective and longitudinal study was conducted over 1 year in 29 children who underwent tonsillectomy due to either chronic tonsillitis or adenotonsillar hypertrophy. Measurements of high‐sensitivity C‐reactive protein (hs‐CRP) levels were taken. Levels of Th1‐type cytokines [interleukin‐1, interferon‐γ, and tumor necrosis factor‐Î± (TNF‐α)] and anti‐inflammatory Th2‐type cytokines [interleukin‐4, ‐5, ‐6, ‐10 and ‐13] were measured. Levels of transforming growth factor‐beta (TGF‐β) and intercellular adhesion molecule‐1 (ICAM‐1) were also determined. The results were compared to those of 29 control children. Results At baseline, children with surgery indications presented with higher levels of hs‐CRP, interleukin‐1 and ‐10, interferon‐γ, TNF‐α and ICAM‐1, whereas values of interleukin‐4 were significantly lower than in control children. Children with severe tonsillar obstruction had higher values of interleukin‐1, ‐4, and ‐5 and lower values of interleukin‐10 compared with children with recurrent tonsillitis. One year after surgery, the levels except IL‐4 did not show a significant difference from those obtained in the control group. The levels of hs‐CRP and TNF‐α decreased significantly in the first month. Conclusion Children with chronic tonsillitis and/or adenotonsillar hypertrophy have significantly elevated levels of proinflammatory cytokines. Adenotonsillectomy restores the normal values of these parameters 1 year after surgery.

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Section: Discussionmentioning

confidence: 99%

Impact of adenotonsillectomy on the evolution of inflammatory markers

Marcano-Acuña

Carrasco-Llatas

Tortajada‐Girbés

et al. 2019

Clinical Otolaryngology

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“…Mattila et al . 31 reported that the proportion of B cells producing immunoglobulin decreases with ageing in adenotonsillar tissues, particularly in adenoids. Age-related decreases coincide with decreased B-cell population or production of immunoglobulin.…”

Section: Discussionmentioning

confidence: 99%

Expression and subcellular localisation of AID and APOBEC3 in adenoid and palatine tonsils

Seishima

Kondo

Wakae

et al. 2018

Sci Rep

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Activation-induced cytidine deaminase (AID) and apolipoprotein B mRNA-editing catalytic polypeptide 3 (A3) family are cytidine deaminases that play critical roles in B-cell maturation, antiviral immunity and carcinogenesis. Adenoids and palatine tonsils are secondary lymphoid immune organs, in which AID and A3s are thought to have several physiological or pathological roles. However, the expression of AID or A3s in these organs has not been investigated. Therefore, we investigated the expression profiles of AID and A3s, using 67 samples of adenoids and palatine tonsils from patients, with reverse transcription quantitative polymerase chain reaction (RT-qPCR) and immunohistochemical analyses. AID and A3s expression levels in the adenoids and the palatine tonsils of the same individual significantly correlated with each other. Of note, AID expression level in the adenoids negatively correlated with the age (r = −0.373, P = 0.003). The younger group with adenoid vegetation and tonsillar hypertrophy showed more abundant AID expression than the older group with recurrent tonsillitis and peritonsillar abscesses (P = 0.026). Moreover, immunohistochemical analysis revealed the distribution of AID and A3s in the epithelial cells as well as germinal centres. The localisation of AID expression and its relation to age may contribute to adenoid vegetation and inflammation.

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“…[ 18 – 20 ] In hypertrophic tonsils, the increase in T and B cell counts showed a positive correlation with bacterial counts and tonsil size. [ 21 , 22 ] In epidemiologic studies, smoking, allergies and recurrent respiratory infections might associate with transient or permanent hypertrophy of lymphoid tissue. [ 22 , 23 ] Immunologic parameters, genetic predisposition and local lymphocyte dysfunction appear to play a role in the etiology of recurrent tonsillitis and tonsillar hypertrophy.…”

Section: Discussionmentioning

confidence: 99%

“…[ 21 , 22 ] In epidemiologic studies, smoking, allergies and recurrent respiratory infections might associate with transient or permanent hypertrophy of lymphoid tissue. [ 22 , 23 ] Immunologic parameters, genetic predisposition and local lymphocyte dysfunction appear to play a role in the etiology of recurrent tonsillitis and tonsillar hypertrophy. [ 22 , 24 ] Some studies demonstrated that tonsillar hypertrophy was associated with increased lymphoid follicle size, but not the number of follicles[ 25 ] and was also related to increased tonsil weight, increased follicle diameter, area and number.…”

Section: Discussionmentioning

confidence: 99%

Extra-Esophageal Pepsin from Stomach Refluxate Promoted Tonsil Hypertrophy

et al. 2016

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BackgroundGastroesophageal reflux is associated with numerous pathologic conditions of the upper aerodigestive tract. Gastric pepsin within reflux contributes to immunologic reactions in the tonsil. In this study, we aimed to find the relationships between pepsin and tonsillar hypertrophy.Methods and findingWe explored the notion whether tonsillar hypertrophy was due to pepsin-mediated gastric reflux in tonsil hypertrophy. Fifty-four children with tonsil hypertrophy and 30 adults with tonsillitis were recruited before surgical treatment. Blood and tonsil tissues from each patient were harvested for analysis of changes in lymphocyte and macrophage numbers coupled with histological and biochemical analysis. Pepsin was expressed at different levels in tonsil tissues from each tonsillar hypertrophy. Pepsin-positive cells were found in the crypt epithelium, surrounding the lymphoid follicle with developing fibrosis, and also surrounding the lymphoid follicle that faced the crypt. And also, pepsin staining was well correlated with damaged tonsillar squamous epithelium and TGF-β1 and iNOS expression in the tonsil section. In addition, pepsin and TGF-β1-positive cells were co-localized with CD68-positive cells in the crypt and surrounding germinal centers. In comparison of macrophage responsiveness to pepsin, peripheral blood mononuclear cells (PBMNCs) were noticeably larger in the presence of activated pepsin in the child group. Furthermore, CD11c and CD163-positive cells were significantly increased by activated pepsin. However, this was not seen for the culture of PBMNCs from the adult group.ConclusionsThe lymphocytes and monocytes are in a highly proliferative state in the tonsillar hypertrophy and associated with increased expression of pro-inflammatory factors as a result of exposure to stomach reflux pepsin.

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Apoptosis in chronic tonsillitis and tonsillar hypertrophy

Cited by 23 publications

References 25 publications

Impact of adenotonsillectomy on the evolution of inflammatory markers

Impact of adenotonsillectomy on the evolution of inflammatory markers

Expression and subcellular localisation of AID and APOBEC3 in adenoid and palatine tonsils

Extra-Esophageal Pepsin from Stomach Refluxate Promoted Tonsil Hypertrophy

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