<p>Detection of pepsin and IL-8 in saliva of adult asthmatic patients</p>

Abstract

Objective: Asthma and gastric reflux disease are widespread and often coexisting diseases with complex interactions, leading some to suspect that asthma symptoms of patients with reflux may improve with anti-reflux therapy. The objective of this study was to determine whether pepsin in saliva, indicative of airway reflux, could be detected in patients with asthma of varying severity and test the requirement of citric acid as a pepsin preservative. Methods: Saliva samples were collected in the clinic (with/without citric acid) and upon waking the following morning from 25 asthmatic patients. Enzyme-linked immunosorbent assay was performed for pepsin and interleukin-8 (IL-8), an inflammatory cytokine induced by pepsin in other airway epithelia. Pepsin induction of IL-8 was tested in a lung epithelial cell culture model. Results: Pepsin was detected in saliva from 14/25 patients (56%; mean concentration of pepsin in specimens where observed ±SD =80.3±87.5 ng/mL); significant agreement was found between samples collected in the presence/absence of citric acid. No significant associations were found with pepsin and clinical measures of asthma severity. IL-8 was detected in saliva from 22/25 patients (88%; mean IL-8 in all specimens where observed =3.27±3.91 ng/mL). IL-8 was significantly upregulated in human lung epithelial cells exposed to pepsin at pH7 in vitro ( P =0.041). Conclusion: In summary, more than half of the asthma patients in this study were found to have pepsin in their saliva, indicative of airway reflux. These data support the use of salivary pepsin as a noninvasive tool for future investigation of airway reflux in a larger cohort. The data further suggest that collection in citric acid as a sample preservative is not warranted and that pooling of multiple saliva samples collected at various timepoints may improve sensitivity of pepsin detection and reduce costs incurred by multiple sample analysis in future studies.

Do Laryngologists and General Otolaryngologists Manage Laryngopharyngeal Reflux Differently?

“…The current survey reveals similar lack of awareness of the potential role of LPR in development of laryngotracheal stenosis and chronic media otitis, despite an increasing literature which supports this relationship. 10,11,26,27 Surprisingly, non-laryngologists seem to be unaware about the role of LPR in bronchial diseases such as asthma; however, many studies have demonstrated that LPR is involved in the development of bronchial hypersensitivity conditions, such as asthma, 28,29 or chronic obstructive pulmonary disease. 30 In the current survey, the largest differences between laryngologists and non-laryngologists concern diagnostic approach towards LPR, particularly with regard to examinations such as esophagoscopy and MII-pH.…”

Syntropy of bronchial asthma and gastroesophageal reflux disease: pathogenetic features and possibilities of minimally invasive diagnostics at the outpatient stage

“…До последнего времени исследования, обосновывающие возможность считать пепсин суррогатным биомаркером ГЭРБ, не остаются без внимания научного сообщества [30,57]. Однако в некоторых работах не было выявлено существенной связи между значениями пепсина слюны и тяжестью клинических проявлений БА [41,58]. Более того, в исследовании Race С. et al было показано, что слюнный пепсин не является надежным инструментом для диагностики ГЭРБ [59].…”

Pepsin and the Lung—Exploring the Relationship between Micro-Aspiration and Respiratory Manifestations of Gastroesophageal Reflux Disease

“…On the other hand, a study by Marshall et al performed on 25 asthmatic patients showed no significant correlation between salivary pepsin levels and clinical measures of asthma severity [ 26 ]. However, one of the major drawbacks of salivary pepsin assessment is the current lack of an optimal timeframe for sample collection.…”