Objective To explore the effect of lower airway inflammation on the pathogenesis of upper airway cough syndrome( UACS) . Methods Ten cases of UACS and 10 cases of chronic rhinitis or sinusitis without cough were enrolled as group A and group B, respectively. And 10 healthy volunteers were included as controls( group C) . The cough threshold C2 and C5 to inhaled capsaicin, defined as the lowest concentration of capsaicin required to induce ≥2 and ≥5 coughs, was measured. The total and differential cell counts was determined in induced sputum, and the levels of histamine and prostaglandin E2 were analyzed in supernatant of sputum. Results Cough threshold was significantly lower in group A than group B [ C2: ( 0.65 ±0. 08) μmol / L vs ( 3.90 ±1. 37) μmol / L; C5: ( 1.59 ±0. 28) μmol / L vs ( 33.46 ±23. 71) μmol / L, P lt;0. 05] and comparable between group B and group C( P gt; 0. 05) . Group A, similar to group B( P gt; 0. 05 ) , contained more inflammatory cells, with decreased percentage of macrophages and increased percentage of neutrophils in induced sputum than group C( P lt; 0. 05) . Furthermore, the levels of histamine[ ( 9. 55 ±1. 89) ng/mL vs ( 2. 37 ±0. 25) ng/mL, P lt; 0. 05] and prostaglandin E2 [ ( 361. 71 ±39. 38) pg/mL vs ( 144. 34 ±15. 69) pg/mL, P lt; 0. 05] were higher in supernatant of induced sputum from group A than group B, while the latter was not different from group C( P gt; 0. 05) . Conclusion Increased cough sensitivity caused by airway inflammation may be important for the pathogenesis of UACS, and the activation of mast cells in mucosa of lower airway might be an important factor.
Citation：
SHI Cuiqin,YU Li,WEI Weili,HUANG Yang,LV Hanjing,QIU Zhongmin.. Effect of Airway Inflammation on Pathogenesis of Upper Airway Cough Syndrome. Chinese Journal of Respiratory and Critical Care Medicine, 2009, 09(3): 256-258. doi:
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- 1. Pratter MR. American College of Chest Physicians( ACCP) . Chronic upper airway cough syndrome secondary to rhinosinus diseases ( previously referred to as postnasal drip syndrome) : ACCP evidencebased clinical practice guidelines. Chest, 2006, 129:63S-71S.
- 2. Hsu JY, Stone RA, Logan-Sinclair RB, et al. Coughing frequency in patients with persistent cough: assessment using a 24 hour ambulatory recorder. Eur Respir J, 1994, 7: 1246-1253.
- 3. 时翠芹, 邱忠民, 吕寒静, 等. 辣椒素咳嗽敏感性试验在慢性咳嗽中的应用价值. 中华结核和呼吸杂志, 2007, 30: 954-966.
- 4. Brightling CE, Ward R, Woltmann G, et al. Induced sputum inflammatory mediator concentrations in eosinophilic bronchitis and asthma. Am J Respir Crit Care Med, 2000, 162: 878-882.
- 5. Tanaka S, Hirata K, Kurihara N, et al. Effect of loratadine, an H1 antihistamine, on induced cough in non-asthmatic patients with chronic cough. Thorax, 1996, 51: 810-814.
- 6. Bonay M, Neukirch C, Grandsaigne M, et al. Changes in airway inflammation following nasal allergic challenge in patients with seasonal rhinitis. Allergy, 2006, 61: 111-118.
- 7. Irwin RS, Ownbey R, Cagle PT, et al. Interpreting the histopathology of chronic cough: a prospective, controlled, comparative study.Chest, 2006, 130: 362-370.
- 8. Nightingale JA, Rogers DF, Barnes PJ. Effect of repeated sputum induction on cell counts in normal volunteers. Thorax,1998, 53: 87-90.
- 9. McGarvey LP, Forsythe P, Heaney LG, et al. Bronchoalveolar lavage findings in patients with chronic nonproductive cough. Eur Respir J,1999, 13: 59-65.
- 10. Marshall JS. Mast-cell responses to pathogens. Nat Rev Immunol,2004, 4: 787-799.
- 11. Niimi A, Chung KF. Airway inflammation and remodeling changes in patients with chronic cough: do they tell us about the cause of cough? Pulm Pharmacol Ther, 2004, 17: 441-446.
