interleukin-8 and Laryngopharyngeal-Reflux

Laryngopharyngeal reflux is a controversial but increasingly made diagnosis used in patients with a collection of often non-specific laryngeal symptoms. It is a clinical diagnosis, and its pathophysiology is currently poorly understood. Previous reflux research has focused on injurious agents, acid, pepsin and biomarker expression. Failure of intrinsic defences in the larynx may cause changes in laryngeal epithelia, particularly alterations in carbonic anhydrases and E-cadherin. Carbonic anhydrase III levels vary in the larynx in response to laryngopharyngeal reflux, depending on location. Expression of E-cadherin, a known tumour suppressor, is reduced in the presence of reflux. Mucin expression also varies according to the severity of reflux. Further research is required to define the clinical entity of laryngopharyngeal reflux, and to identify a definitive mechanism for mucosal injury. Understanding this mechanism should allow the development of a comprehensive model, which would enable future diagnostic and therapeutic interventions to be developed.

Topics: Adult; Bile Acids and Salts; Biomarkers; Cadherins; Carbonic Anhydrase III; Gastric Acid; Gastroesophageal Reflux; Humans; Interleukin-8; Laryngeal Mucosa; Laryngopharyngeal Reflux; Mucins; Pepsin A; Severity of Illness Index

The aim: To examine the composition of the oral microbiome in young children with laryngopharyngeal reflux (LPR) and its role the development of recurrent respiratory diseases.. Materials and methods: There were examined 38 children with physiological gastroesophageal reflux (GER), 18 children with LPR who had a medical history of recurrent bronchitis and 17 healthy children (control group). The study included the collection of anamnesis, objective examination. The qualitative and quantitative microbial composition of the upper respiratory tract was performed obtained by oropharyngeal deep swab. Salivary pepsin level and IL-8 were determined by enzyme-linked immunosorbent assay.. Results: This research showed significant alterations in the oral microbiome of patients with GER and LPR as compared to healthy control. We found that gram-negative microbiota such as Klebsiella pneumoniae, Escherichia coli, Proteus vulgaris, Proteus spp. and Candida albicans were identified in children with GER and LPR compared to the healthy control. At the same time, the amount of such a representative of the normal microbiome as Streptococcus viridans in children with LPR was sharply reduced. There were established a much higher mean salivary pepsin level of the patients with LPR than in the GER and control group. We found the association between high pepsin levels, saliva IL-8 levels and frequency of respiratory pathology in children with LPR.. Conclusions: Our study confirms that increased levels of pepsin in saliva are a risk factor for recurrent respiratory diseases in children with LPR.

Topics: Bronchitis; Child; Child, Preschool; Gastroesophageal Reflux; Gastrointestinal Microbiome; Humans; Interleukin-8; Laryngopharyngeal Reflux; Mouth; Pepsin A; Recurrence; Risk Factors; Saliva

Bacteria infection and laryngopharyngeal reflux (LPR) were believed the important pathogenesis of chronic otitis media with effusion (COME). But no study researched the relationship between them on COME.. To confirm bacterial could arrive middle ear through LPR and produced acid metabolites to activate the pepsinogen of LPR causing COME.. Children (65) diagnosed COME with 122 middle ear effusions were included in COME group. Children (22) with congenital/acquired profound deafness with 22 middle ear lavage were included in CI group. Pepsin A concentration in the effusion and lavage fluid were measured. The DNA of the bacteria, IL-8 and TNF-α in the effusion were detected.. The average concentration of pepsin A in the effusions and lavage were 176.65 ± 242.09 and 19 ng/ml. Bacterial infection rates were 75.76% and 24.24% in the pepsin A(+) and pepsin A(-) patients. In the bacterial (+), the patients of pepsin A(+) was 4.33 times higher than those of pepsin A(-). TNF-α in pepsin A(+) was higher than that in pepsin A(-). TNF-α and IL-8 were higher in bacteria(+) than those of bacteria(-).. Bacterial infection and LPR might act in synergy in the pathogenesis of COME.. First time to propose LPR and bacterial infection might work synergistically to cause COME.

Topics: Adolescent; Bacterial Infections; Child; Child, Preschool; Chronic Disease; Cochlear Implants; Deafness; Ear, Middle; Female; Humans; Interleukin-8; Laryngopharyngeal Reflux; Male; Middle Ear Ventilation; Otitis Media with Effusion; Pepsin A; Prospective Studies; Tumor Necrosis Factor-alpha

Laryngomalacia is a common cause of stridor in infants and is associated with laryngopharyngeal reflux (LPR). Although pepsin in operative supraglottic lavage specimens is associated with severe laryngomalacia, detection of pepsin in oral secretions has not been demonstrated in an outpatient setting.. Children <2 years old with laryngomalacia diagnosed by flexible laryngoscopy and children without stridor were selected. Oral secretion samples were obtained in clinic from all subjects. Pepsin, IL-1β, and IL-8 enzyme-linked immunosorbent assays were performed to determine presence of LPR.. Sixteen laryngomalacia and sixteen controls were enrolled. Pepsin was detected more frequently in oral secretions of patients with laryngomalacia (13/16) than in controls (2/16;. Pepsin in saliva appears to be associated with laryngomalacia, suggesting a role for salivary pepsin as a noninvasive marker of LPR in patients with laryngomalacia. Future studies will determine the utility of this test in laryngomalacia.

Topics: Biomarkers; Case-Control Studies; Enzyme-Linked Immunosorbent Assay; Female; Humans; Infant; Interleukin-1beta; Interleukin-8; Laryngomalacia; Laryngopharyngeal Reflux; Laryngoscopy; Male; Pepsin A; Respiratory Sounds; Saliva