Innate immunity gene expression by epithelial cells of upper respiratory tract in children with adenoid hypertrophy

Gankovskaya, L. V.; Быкова, В. П.; Namasova-Baranova, Leila Seimurovna; Karaulov, Alexander; Rahmanova, Irina Viktorovna; Ганковский, В. А.; Merkushova, Catherine Dmitrievna; Свитич, О. А.

doi:10.1016/j.anl.2017.11.011

Cited by 7 publications

(7 citation statements)

References 8 publications

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“…Recognition of pathogens and endogenous TLR ligands promotes the activation of genes that encode proinflammatory cytokines, antimicrobial peptides, and other defense molecules [ 46 ]. Upregulation of TLRs has been observed in upper respiratory tract infections [ 47 ].…”

Section: Role Of the Epipharyngeal Lymphoid Tissue In Iganmentioning

confidence: 99%

Role of Palatine Tonsil and Epipharyngeal Lymphoid Tissue in the Development of Glomerular Active Lesions (Glomerular vasculitis) in Immunoglobulin A Nephropathy

Hasegawa¹,

Ieiri²,

Nagai³

et al. 2022

IJMS

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Hematuria is an essential symptom of immunoglobulin A nephropathy (IgAN). Although the etiology of hematuria in IgAN has not been fully elucidated, it is thought that the rupture of the glomerular basement membranes caused by intra-capillary leukocyte influx, so-called glomerular vasculitis, is the pathological condition responsible for severe hematuria. Glomerular vasculitis are active lesions that exist in the glomeruli of acute phase IgAN and it is important because it is suspected to make the transition to segmental glomerular sclerosis (SGS) as a repair scar lesion in the chronic phase, and the progression of SGS would eventually lead to glomerular obsolescence. Worsening of hematuria concomitant with acute pharyngitis is common in patients with IgAN; therefore, elucidating the relationship between the immune system of Waldeyer’s ring, including the palatine tonsil and epipharyngeal lymphoid tissue, and the glomerular vasculitis may lead to understanding the nature of IgAN. The epipharynx is an immunologically activated site even under normal conditions, and enhanced activation of innate immunity is likely to occur in response to airborne infection. Hyperactivation of innate immunity via upregulation of Toll-like receptors in the interfollicular area of the palatine tonsil and epipharyngeal lymphoid tissue, followed by enhanced fractalkine/CX3CR1 interactions, appears to play an important role in the development of glomerular vasculitis in IgAN. As latent but significant epipharyngitis is present in most patients with IgAN, it is plausible that acute upper respiratory infection may contribute as a trigger for the innate epipharyngeal immune system, which is already upregulated in a chronically inflamed environment. Given that epipharyngitis and its effects on IgAN are not fully understood, we propose that the so-called “epipharynx–kidney axis” may provide an important focus for future research.

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Section: Role Of the Epipharyngeal Lymphoid Tissue In Iganmentioning

confidence: 99%

Role of Palatine Tonsil and Epipharyngeal Lymphoid Tissue in the Development of Glomerular Active Lesions (Glomerular vasculitis) in Immunoglobulin A Nephropathy

Hasegawa¹,

Ieiri²,

Nagai³

et al. 2022

IJMS

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“…Adenoid hypertrophy (AH), the most common cause of upper airway obstruction (AO) in children and adolescents, is a natural response to the increase of immune activity in childhood [ 1 , 2 ]. The normal breathing pattern of human beings is nasal respiration, which means that air travels through the nasal, nasopharyngeal, oropharyngeal, and laryngopharyngeal cavity into the lower airway [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

Influences of Airway Obstruction Caused by Adenoid Hypertrophy on Growth and Development of Craniomaxillofacial Structure and Respiratory Function in Children

Wang

Hao

et al. 2022

Computational and Mathematical Methods in Medicine

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Adenoid hypertrophy (AH) is a common disease in otorhinolaryngology. Children with chronic snoring and hypoxia are susceptible to long-term nasal obstruction, while long-term open-mouth breathing may cause craniofacial bone development disorders and dull facial expressions, the so-called adenoid face. The purpose of this work is to analyze the influence of AH-induced airway obstruction (AO) on the growth and development of craniomaxillofacial structure and respiratory function (RF) in children. The clinical data of 56 AH children (observation group) and 42 healthy children with physical examination (control group) who visited the Hebei Eye Hospital during the same period were retrospectively analyzed. All children received acoustic rhinometry and X-ray cephalometric measurements. The upper airway structure, sleep disorder score, and A / N value of nasopharyngeal lateral X-ray images were compared between cases and controls. For AH children, sleep tests were also performed to assess their RF. X-ray cephalometric measurements of facial morphology showed obvious vertical growth, mandibular retrognathia, and enlarged mandibular angle in AH children. AH mainly affects the size of the nasopharyngeal and oropharyngeal airway. AH children presented with higher nasal airway resistance ( 5.11 ± 1.95 cmH2O/L min) and lower nasopharyngeal volume (NPV) ( 16.86 ± 3.93 cm3) than controls. Of the AH children, 45 had abnormal RF, including 4 with obstructive sleep apnea syndrome. The A / N value of nasopharyngeal lateral X-ray images was significantly higher in AH children than in controls. Besides, worse sleep quality was found in AH children. The above differences were all of statistical significance. The above indicates that AH can affect the size of the nasopharyngeal and oropharyngeal airway, change children’s respiratory mode and RF, increase nasal resistance, and decrease NPV, resulting in upper respiratory tract stenosis, as well as craniomaxillofacial and oral malformations, which affects children’s normal growth and development.

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“…A few studies exist in the literature as regards to the association between TLR activation in neutrophils and their HNP expression. Over‐expressions of genes TLR2 and TLR4 were related to suppressed gene expression of hBD‐1 , hBD‐2 , and HNP‐1 in children with adenoid hypertrophy (Gankovskaya et al, 2018). Surprisingly, it has been shown that Vitamin D increased pneumococcal killing of neutrophils by stimulating the HNP protein expression via TLR2 activation (Subramanian et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

Toll‐like receptor‐1, ‐2, and ‐6 genotypes in relation to salivary human beta‐defensin‐1, ‐2, ‐3 and human neutrophilic peptide‐1

Gürsoy

Könönen

et al. 2022

J Clinic Periodontology

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Aim To examine whether functional gene polymorphisms of toll‐like receptor (TLR)1, TLR2, and TLR6 are related to the salivary concentrations of human beta‐defensins (hBDs)‐1, ‐2, ‐3, and human neutrophilic peptide (HNP)‐1. Materials and Methods Polymorphisms of TLR1 (rs5743618), TLR2 (rs5743708), and TLR6 (rs5743810) were genotyped by PCR‐based pyrosequencing from the salivary samples of 230 adults. Salivary hBD‐1, ‐2, ‐3, and HNP‐1 concentrations were measured using enzyme‐linked immunosorbent assay. General and periodontal health examinations, including panoramic radiography, were available for all participants. Results The genotype frequencies for wild types and variant types were as follows: 66.5% and 33.5% for TLR1, 95.5% and 4.5% for TLR2, and 25.1% and 74.9% for TLR6, respectively. The TLR2 heterozygote variant group exhibited higher salivary hBD‐2 concentrations than the TLR2 wild‐type group (p = .038). On the contrary, elevated hBD‐2 concentrations were detected in the TLR6 wild‐type group compared with the TLR6 heterozygote and homozygote variant group (p = .028). The associations between TLR6 genotypes and salivary hBD‐2 concentrations remained significant after adjusting them for periodontal status, age, and smoking. Conclusion hBD‐2 concentrations in saliva are related to TLR2 and TLR6 polymorphisms, but only the TLR6 genotype seems to exhibit an independent association with the salivary hBD‐2 concentrations.

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Innate immunity gene expression by epithelial cells of upper respiratory tract in children with adenoid hypertrophy

Cited by 7 publications

References 8 publications

Role of Palatine Tonsil and Epipharyngeal Lymphoid Tissue in the Development of Glomerular Active Lesions (Glomerular vasculitis) in Immunoglobulin A Nephropathy

Role of Palatine Tonsil and Epipharyngeal Lymphoid Tissue in the Development of Glomerular Active Lesions (Glomerular vasculitis) in Immunoglobulin A Nephropathy

Influences of Airway Obstruction Caused by Adenoid Hypertrophy on Growth and Development of Craniomaxillofacial Structure and Respiratory Function in Children

Toll‐like receptor‐1, ‐2, and ‐6 genotypes in relation to salivary human beta‐defensin‐1, ‐2, ‐3 and human neutrophilic peptide‐1

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