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PubMed2005

How does lobeline injected intravenously produce a cough?

In order to examine, whether the lobeline-induced cough is a true reflex or a voluntary effort to get rid of its irritating sensations in the upper respiratory tract, we systematically studied the cough response to lobeline, of subjects who were unable to make conscious discriminations i.e. were either comatose (n=4) or anaesthetized (n=5). 8 microg/kg lobeline injected into the right atrium of one and 29 microg/kg intravenously (i.v.) into another evenly and spontaneously breathing comatose subject produced a cough after 4s and 12s, respectively. Cough was repeatable and showed a dose response relationship i.e., its latency decreasing and its duration/intensity increasing with the dose. In a third subject, capable only of weak spontaneous respiration, a relatively high dose injected into the right atrium (44 microg/kg) generated a pronounced cough-like respiratory movement superimposed on the artificial ventilation and also during the apnoea after disconnecting the pump. No respiratory response was evoked in a fourth subject who had no evidence of brainstem reflexes. In five normals, cough was elicited with a mean dose of 35+/-5 microg/kg i.v. (latency 14+/-2 s; duration 10+/-3 s). After thiopental anaesthesia, injecting 41+/-7 microg/kg produced a cough within 13+/-2 s that lasted for 12+/-2 s. It may be noted that neither the later dose nor the latency or duration of cough that it produced were significantly different from the pre anaesthesia values (P>0.05). These two sets of results show unequivocally that the lobeline-induced cough is evoked reflexly; its magnitude in the conscious state could vary by subjective influences. We discuss the likelihood of its origin from juxtapulmonary capillary receptors.

Adult↗
PubMed2006

Neurogenesis of cough, other airway defensive behaviors and breathing: A holarchical system?

Cough and breathing are generated by a common muscular system. However, these two behaviors differ significantly in their mechanical features and regulation. The current conceptualization of the neurogenic mechanism for these behaviors holds that the multifunctional respiratory pattern generator undergoes reconfiguration to produce cough. Our previous results indicate the presence of a functional cough gate mechanism that controls the excitability of this airway defensive behavior, but is not involved in the regulation of breathing. We propose that the neurogenesis of cough, breathing, and other nonbreathing behaviors is controlled by a larger network, of which the respiratory pattern generator is part. This network we term a holarchical system. This system is governed by functional control elements known as holons, which confer unique regulatory features to each behavior. The cough gate is an example of such a holon. Neurons that participate in a cough holon may include behavior selective elements. That is, neurons that are either specifically recruited during cough and/or tonically-active neurons with little or no modulation during breathing but with significant alterations in discharge during coughing. We also propose that the holarchical system is responsible for the orderly expression of different airway defensive behaviors such that each motor task is executed in a temporally and mechanically discrete manner. We further propose that a holon controlling one airway defensive behavior can regulate the excitability of, and cooperate with, holons unique to other behaviors. As such, co-expression of multiple rhythmic behaviors such as cough and swallow can occur without compromising airway defense.

Animals↗
PubMed2006

Vagal afferent nerves regulating the cough reflex.

Coughing is initiated by activation of mechanically and chemically sensitive vagal afferent nerves innervating the airways. All afferent nerve subtypes innervating the airways can modulate the cough reflex. Rapidly adapting and slowly adapting stretch receptors (RARs and SARs, respectively) innervating the intrapulmonary airways and lung may enhance and facilitate coughing. Activation of intrapulmonary C-fibers has been shown to inhibit coughing in anesthetized animals. Extrapulmonary C-fibers and RARs can initiate coughing upon activation. C-fiber-dependent coughing is uniquely sensitive to anesthesia. Tracheal and bronchial C-fibers may also interact with other afferents to enhance coughing. Recent studies in anesthetized guinea pigs have identified a myelinated afferent nerve subtype that can be differentiated from intrapulmonary RARs and SARs and play an essential role in initiating cough. Whether these "cough receptors" are the guinea pig equivalent of the irritant receptors described in the extrapulmonary airways of other species is unclear.

Afferent Pathways↗
PubMed1999

The association of chronic cough with the risk of myocardial infarction: the Framingham Heart Study.

PURPOSE: A persistent inflammatory response accompanying chronic infections may contribute to the risk of coronary atherothrombosis. Recent studies have reported an association between chronic respiratory infections and an increased risk of coronary heart disease; however, these reports have not accounted for important confounders such as impaired lung function. METHODS: We considered chronic cough as an indicator of chronic lung infection or inflammation in the original Framingham Heart Study participants aged 47 to 89 years. Chronic cough was defined as a cough present for at least 3 months in the preceding year and was categorized as either nonproductive or productive. The association of chronic cough with myocardial infarction was examined for six consecutive examination cycles (1965 to 1979) among participants free of myocardial infarction at the baseline examination. In a secondary analysis, plasma fibrinogen levels were measured during examination cycle 10 (1965 to 1967) in a subgroup of the study sample (n = 1,288). Multivariable logistic regression analysis was performed adjusting for age, gender, smoking status, forced vital capacity, and other known risk factors. RESULTS: The cross-sectional pooling method yielded 15,656 person-examinations in 3,637 subjects. During follow-up, there were 291 incident myocardial infarctions. Chronic nonproductive cough (odds ratio [OR] 1.8, 95% confidence interval [CI] 1.1 to 2.8) and chronic productive cough (OR 1.6, CI 1.1 to 2.4) were independent predictors of myocardial infarction. Results were unchanged when we further adjusted for a history of heart failure. Adjusted plasma fibrinogen levels (mean +/- SD) were greater in those with chronic nonproductive cough than among those without cough (3.2 +/- 0.6 g/L versus 2.9 +/- 0.6 g/dL, P = 0.001). CONCLUSIONS: These findings provide evidence that chronic cough, a clinical manifestation of pulmonary infection or chronic inflammation, is associated with the risk of myocardial infarction. Acute phase reactants such as plasma fibrinogen may be implicated in this association. Prospective serologic studies of infections as predictors of coronary heart disease risk are warranted.

Aged↗
PubMed2000

The cough reflex and its relation to gastroesophageal reflux.

Each cough involves a complex reflex arc beginning with the stimulation of sensory nerves that function as cough receptors. There is evidence, primarily clinical, that the sensory limb of the reflex exists in and outside of the lower respiratory tract. Although myelinated, rapidly adapting pulmonary stretch receptors (RARs), also known as irritant receptors, are the most likely type of sensory nerve that stimulates the cough center in the brain, afferent C-fibers and slowly adapting pulmonary stretch receptors (SARs) also may modulate cough. RARS, C-fibers, and SARs have been identified in the distal esophageal mucosa; however, studies have not been performed to determine whether they can participate in the cough reflex. Although gastroesophageal reflux disease can potentially stimulate the afferent limb of the cough reflex by irritating the upper respiratory tract without aspiration and by irritating the lower respiratory tract by micro- or macroaspiration, there is evidence that strongly suggests that reflux commonly provokes cough by stimulating an esophageal-bronchial reflex. Theoretically, the pathways of this reflex may be modeled in a variety of ways, and these are speculated upon in this article. The predominant role of acid in triggering cough by means of this reflex is unclear because of conflicting results from provocative challenge studies. It is interesting to speculate that a distal esophageal-bronchial reflex evolved as an early warning defense so that coughing could be started, just in case the refluxate were to reach the inlet of the lower respiratory tract. That is, thinking teleologically, it is possible that an esophageal-bronchial reflex evolved as one of several mechanisms designed to protect the lungs from aspiration of gastric contents.

Bronchi↗
PubMed1997

Differential effect of codeine on coughs caused by mechanical stimulation of two different sites in the airway of guinea pigs.

We studied the difference in the effects of codeine on coughs caused by mechanical stimulation to the larynx and to the bifurcation of the trachea in lightly anaesthetized guinea pigs. Mechanical stimulation to the larynx or the bifurcation of trachea caused a stable cough response. The response was reproducible over 60 min, when stimulation was repeatedly applied at 20-min intervals. No significant difference was found between the amplitudes of the responses to mechanical stimulation of the larynx and of the tracheal bifurcation. Codeine, 10, 20 and 50 mg/kg, dose dependently depressed the coughs caused by larynx stimulation. The antitussive, however, failed to depress the cough caused by stimulation to the tracheal bifurcation, although a large dose, 50 mg/kg, significantly depressed the cough. In capsaicin-treated guinea pigs, codeine at 20 mg/kg significantly depressed the cough caused by stimulation to the tracheal bifurcation. The present results suggest that cough caused by mechanical stimulation to the larynx might be more sensitive to codeine treatment than cough caused by stimulation to the bifurcation of trachea. Furthermore, it is suggested that coughs caused by mechanical stimulation to both sites might consist of at least two components as regards their pharmacological nature.

Animals↗
PubMed1997

Thromboxane A2 synthetase inhibition suppresses cough induced by angiotensin converting enzyme inhibitors.

Based on our earlier animal study, we became interested to investigate if thromboxane A2 (TXA2) is involved in angiotensin converting enzyme (ACE) induced cough in man. To 11 patients with hypertension, who had developed cough induced by ACE inhibitors, a TXA2 synthetase inhibitor, ozagrel was given for 1 to 2 months together with the ACE inhibitors. One patient developed headache induced by ozagrel and was eliminated from the study after 3 weeks. In other 10 patients, no obvious drug attributable abnormality was observed in subjective and objective symptoms or laboratory tests. In ten patients, cough scores were taken just before and after the administration of a combination of an ACE inhibitor with ozagrel. Median values of cough scores after the combination was significantly (p=0.012) lower than before the combination. Ozagrel reduced cough scores in 5 patients, completely suppressed cough in 3 patients and in 2 of 10 patients, ozagrel did not affect cough scores. Our observations suggest that TXA2 may somehow, mediate coughing induced by the ACE inhibitors. Further, patients on ACE inhibitors who develop cough may benefit from TXA2 synthetase inhibitors.

Adult↗
PubMed2001

Chronic tobacco smoke exposure increases cough to capsaicin in awake guinea pigs.

Chronic exposure to irritants such as tobacco smoke (TS) can induce spontaneous and enhanced irritant-induced coughing, especially in asthma. To determine if the mechanism of enhanced coughing involves activation of capsaicin-sensitive sensory receptors (C-fibers), we exposed both non-sensitized (NS) and ovalbumin-sensitized guinea pigs to TS (5 mg/L air, 30 min exposure, and 7 days/week). Similar groups were exposed to compressed air. After 90 days of exposure, we challenged the airways with capsaicin, bradykinin, histamine and methacholine. Capsaicin induced coughing as well as bronchoconstriction in guinea pigs exposed to TS. In ovalbumin (OA) guinea pigs coughing and bronchoconstriction were enhanced. Tachykinin receptor antagonists attenuated coughing to both capsaicin and acute TS challenge. Bradykinin also induced coughing and bronchoconstriction in guinea pigs exposed to TS. There was no statistical separation between the two TS groups however. Histamine and methacholine induced similar bronchoconstriction but fewer coughs in all four experimental groups. In conclusion, chronic TS exposure induced coughing to capsaicin and bradykinin challenge. The effect of capsaicin was further enhanced in OA guinea pigs. Enhanced coughing induced by TS exposure likely involves activation of capsaicin-sensitive sensory C-fibers and neuropeptide release with possible subsequent activation of rapidly-adapting receptors.

Aerosols↗
PubMed1998

Extrathoracic airway dysfunction in cough associated with gastroesophageal reflux.

BACKGROUND: Cough associated with gastroesophageal reflux (GER) may originate in extrathoracic airway receptors made hypersensitive by acid-induced mucosal injury. OBJECTIVE: We investigated the role of laryngeal disease and dysfunction in the pathogenesis of GER-associated cough in nonasthmatic patients. METHODS: Seven patients with GER-associated cough were compared with 7 patients with GER but no cough. The patients underwent fiberoptic endoscopy for assessment of laryngitis and esophagitis (expressed by scores); esophageal manometry; 24-hour pH monitoring; lung function tests; and histamine inhalation challenge with assessment of bronchial threshold (concentration provoking 10% fall in FEV1 [PC10]), extrathoracic airway threshold (concentration provoking 25% fall in the maximal midinspiratory flow [PC25MIF50]), and cough threshold (concentration provoking 5 or more coughs PCcough). The patients were reevaluated after 3 months of medical treatment for GER. RESULTS: Patients with cough, compared with those without cough, had significantly higher laryngitis scores (P = .002), lower esophageal sphincter pressures, longer time with pH below 4 (P = .003), greater number of episodes of reflux longer than 5 minutes (P = .016), longer esophageal clearance time (P = .048), and significantly lower PC25MIF50 (P = .005) and PCcough (P = .008) values. Laryngitis score was significantly inversely related to either PCcough (P < .001) or PC25MIF50 (P <.01) but not to PC10. Laryngitis score, PC25MIF50, and PCcough were all closely related to GER severity. After GER treatment, laryngitis, PC25MIF50, and PCcough were all significantly improved. CONCLUSIONS: These findings suggest that GER-associated cough is strongly associated with laryngeal disease and dysfunction consequent to acid reflux injury in nonasthmatic patients.

Adult↗
PubMedDate not supplied

Use of losartan in the treatment of hypertensive patients with a history of cough induced by angiotensin-converting enzyme inhibitors.

The objective of this study was to determine the incidence of dry cough in hypertensive patients with a history of angiotensin-converting enzyme (ACE) inhibitor-induced cough after treatment with losartan (an angiotensin II-receptor antagonist), lisinopril (an ACE inhibitor), or placebo. One hundred patients from 16 outpatient treatment centers in the United States were included in this double-masked, randomized, parallel-group, active- and placebo-controlled study, with stratification according to sex. After a challenge phase with lisinopril and a placebo washout phase, patients were randomly allocated to receive losartan 50 mg once daily, lisinopril 20 mg once daily, or placebo for a maximum of 8 weeks. The primary efficacy end point of the study was the presence or absence of dry cough during the double-masked period, as rated by the patient at each visit using a validated symptom assessment questionnaire. A secondary end point was the frequency of dry cough, as measured at each visit using a visual analogue scale (VAS). The incidence of dry cough was significantly higher in the lisinopril group than in the losartan and placebo groups (87.5% vs 36.7% and 31.4%, respectively) at the end of the double-masked treatment period; there was no statistically significant difference between the losartan and placebo groups. Mean VAS scores showed that patients treated with lisinopril rated themselves as having a significantly higher frequency of cough than did patients treated with losartan or placebo (4.0 vs 1.2 and 1.5, respectively). Again, the difference between the losartan and placebo groups was not statistically significant. All treatments were otherwise well tolerated, and no serious clinical or laboratory adverse events were reported during the double-masked phase of the study. These results demonstrate that the incidence, severity, and frequency of dry cough in patients with a history of ACE inhibitor-induced dry cough are significantly lower in those treated with losartan than in those treated with lisinopril and are similar to the incidence, severity, and frequency of dry cough in those receiving placebo.

Adult↗
PubMed2004

[Chronic cough in childhood].

INTRODUCTION: Although less frequent than viral induced recurrent cough; chronic cough remains a sometimes difficult to resolve diagnostic tool. STATE OF THE ART: Most authors estimate that a cough can by considered as chronic after three weeks of duration. Few papers have been published concerning etiologic diagnosis of chronic cough in childhood but these indicate the same main causes as in adults: cough variant asthma, postnasal drip syndrome, gastro-esophageal reflux. Nevertheless, each age bracket presents specific diagnosis: malformations between zero and one year, psychogenic cough in adolescents. PERSPECTIVES: New techniques as induced sputum studies helps to refine chronic cough diagnosis in childhood (after 7 years). Eosinophilic bronchitis, associated or not to bronchial hyperresponsiveness has important therapeutic consequences because associated with a favourable response to corticosteroids. Other techniques will be developed in the future (exhaled NO for example). CONCLUSIONS: Chronic cough in childhood must be investigated from an anatomic point of view and on frequency arguments. Control and removal of the cough will only be obtained if a precise diagnosis and a suitable treatment are reached.

Child↗
PubMed1996

Capsaicin cough sensitivity increases during upper respiratory infection.

The mechanism of cough associated with upper respiratory infection (URI) is poorly understood. This paper reports a study of the role of altered sensitivity of capsaicin-sensitive airway nerves. In a prospective study, baseline (B) capsaicin-induced cough and methacholine-induced airway responsiveness were measured in 103 healthy volunteers. During the following year, 31 subjects reattended for challenge testing during URI (I) and after recovery (R). The log concentration of capsaicin required to elicit two coughs (C2) was significantly lower during infection than recovery but not baseline [median (interquartile range) B = 0.59 (0.28-1.20), I = 0.27 (0-0.89), R = 0.89 (0.28-1.49)]. Log C5 (concentration causing five coughs) was lower during infection than baseline and recovery [B = 1.79 (1.20-2.70), I = 1.49 (0.89-2.08), R = 1.79 (1.20-2.40)]. FEV1 and PC15 methacholine values were unchanged during infection compared to baseline. Subjects with dry cough (n = 14) had lower C5 values during infection than both baseline and recovery, and lower C2 values during infection than recovery; in these subjects, increase in capsaicin sensitivity correlated with cough severity score. Subjects with productive cough or no cough showed no consistent changes during infection. Twenty-six control subjects who reattended without URI showed no change in capsaicin sensitivity. Upper respiratory infection may cause cough as a result of increased sensitivity of capsaicin-sensitive afferent airway nerves without affecting airway calibre or responsiveness.

Administration, Inhalation↗
PubMed2000

Airway inflammation, airway responsiveness and cough before and after inhaled budesonide in patients with eosinophilic bronchitis.

Eosinophilic bronchitis is a common cause of chronic cough, characterized by sputum eosinophilia similar to that seen in asthma, but unlike asthma the patients have no objective evidence of variable airflow obstruction or airway hyperresponsiveness. The reason for the different functional associations is unclear. The authors have tested the hypothesis that in eosinophilic bronchitis the inflammation is mainly localized in the upper airway. In an open study the authors measured the lower (provocative concentration causing a 20% fall in forced expiratory volume in one second (PC20)) and upper (PC25 MIF50) airway responsiveness to histamine, lower and upper airway inflammation using induced sputum and nasal lavage, in II patients with eosinophilic bronchitis. The authors assessed changes in these measures and in cough reflex sensitivity to capsaicin and cough severity after 400 microg of inhaled budesonide for 4 weeks. A nasal eosinophilia was present in only three patients with one having upper airway hyperresponsiveness. Following treatment with inhaled corticosteroids the geometric mean sputum eosinophil count decreased from 12.8% to 2.9% (mean difference 4.4-fold, 95% confidence interval (CI) 2.14-10.02), the mean +/- sem cough visual analogue score on a 100 mm scale decreased from 27.2 +/- 6.6 mm to 12.6 +/- 5.7 mm (mean difference 14.6, 95% CI 9.1-20.1) and the cough sensitivity assessed as the capsaicin concentration required to cause two coughs (C2) and five coughs (C5) improved (C2 mean difference 0.75 doubling concentrations, 95% CI 0.36-1.1; C5 mean difference 1.3 doubling concentration, 95% CI 0.6-2.1). There was a significant positive correlation between the fold change in sputum eosinophil count and doubling dose change in C5 after inhaled budesonide (r=0.61). It is concluded that upper airway inflammation is not prominent in eosinophilic bronchitis and that inhaled budesonide improves the sputum eosinophilia, cough severity and sensitivity suggesting a causal link between the inflammation and cough.

Administration, Inhalation↗
PubMed2000

Chronic cough and gastro-oesophageal reflux: a double-blind placebo-controlled study with omeprazole.

Gastro-oesophageal reflux (GOR) is an important cause of chronic cough. There has been a lack of placebo-controlled trials treating GOR related chronic cough with antireflux therapy. The aim of this study was to determine the efficacy of omeprazole on GOR related chronic cough. After excluding other common causes of cough, oesophageal pH monitoring was performed on 48 patients with chronic cough. Twenty-nine patients found to have GOR were randomized in a double-blind fashion to receive omeprazole 40 mg o.d. or placebo for 8 weeks. After a 2-week washout period, patients were crossed over to the other treatment. Symptoms were recorded daily in a diary. Twenty-one patients completed both treatment periods. Cough (p=0.02) and gastric symptoms (p=0.003) improved significantly during the omeprazole treatment in twelve patients who received placebo during the first and omeprazole during the second 8-week period. In nine patients who received omeprazole during the first 8-week period, amelioration in cough reached statistical significance only after cessation of omeprazole. Gastric symptoms also remained minor during placebo in these nine patients. Omeprazole 40 mg o.d. seems to improve chronic cough in patients with gastrooesophageal reflux and the effect of omeprazole in ameliorating both cough and reflux symptoms continues after treatment ceases.

Adult↗
PubMed2000

Participation of thromboxane A(2) in the cough response in guinea-pigs: antitussive effect of ozagrel.

1. The purpose of this study was to investigate the involvement of thromboxane A(2) (TXA(2)) in the cough response in a guinea-pig cough model. Here, we describe results obtained using a selective TXA(2) synthetase inhibitor, ozagrel, and a selective TXA(2) agonist, U-46619. 2. Guinea-pigs were anaesthetized and exposed to an aerosol of capsaicin (100 microM) to elicit coughing. The number of coughs was 20.0+/-5.8 during capsaicin provocation (5 min), but only 2. 8+/-0.4 during a 5-min inhalation of phosphate-buffered saline (PBS) (P:<0.05). 3. TXB(2) levels in BAL were 101.4+/-8.0 and 58.4+/-8.7 pg ml(-1) following capsaicin and PBS inhalation, respectively (P:<0. 01), but there was no intergroup difference in the cell populations in BAL. 4. Inhalation of U-46619 did not induce a cough response by itself at concentrations of 100 ng ml(-1) to 10 microg ml(-1). However, it caused a 2 fold increase in the number of capsaicin-induced coughs. 5. To explore the source of the TXA(2), BAL cells were stimulated with capsaicin and the supernatants collected for analysis. The TXB(2) concentration in BAL was increased dose-dependently, indicating that TXA(2) is released from BAL cells in response to capsaicin. 6. Ozagrel was administered orally 1 h before a 5 min capsaicin provocation and the number of coughs was counted during the capsaicin inhalation. Ozagrel decreased the number of coughs dose-dependently (ED(50) value, 26.3 mg kg(-1)). 7. These results show that TXA(2) modulates the capsaicin-induced cough response by increasing capsaicin-sensitivity.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2002

Association of polymorphisms of the renin-angiotensin system and bradykinin B2 receptor with ACE-inhibitor-related cough.

The use of angiotensin-converting enzyme (ACE) inhibitors to treat hypertension has recently increased. However, their use is associated with a persistent dry cough in a significant percentage of such patients. The present study was designed to assess the contribution of polymorphisms as a genetic marker of ACE-inhibitor-related cough in a Japanese hypertensive population. Genotyping was carried out in 190 patients, 70 with cough and 120 without cough, who had been treated with ACE inhibitors. Polymorphisms of ACE insertion/deletion (I/D), angiotensin II type 1 receptor (1166A/C), type 2 receptor (3123C/A), and bradykinin B2 receptor (-58T/C, exon 1, I/D), were analyzed in these subjects. The TT genotype and T allele of bradykinin B2 receptor (-58T/C) were identified at a significantly higher frequency in the cough (+) patients than in the cough (-) patients. This difference was even more pronounced in women. However, there was no significant relationship between polymorphisms of ACE, angiotensin II receptors, or bradykinin B2 receptor exon 1, and occurrence of ACE-inhibitor-related cough. The transcriptional activity of the bradykinin B2 receptor promoter is involved in the occurrence of cough, and this new marker may provide a valuable tool to detect patients at risk of developing this side effect of ACE inhibitors. In conclusion, Susceptibility to develop cough is associated with a genetic variant of the bradykinin B2 receptor promoter; thus, it may be possible to identify those patients who will develop this adverse reaction to ACE inhibitors in advance.

Adult↗
PubMed1997

Cough in spinal cord injured patients: the relationship between motor level and peak expiratory flow.

Pulmonary complications remain a major cause of morbidity and mortality in patients with higher level spinal cord injury. Neurologically intact individuals can cough in order to clear their air passage of lung secretions and foreign material. Patients with higher level cord injuries, with paralysis of the trunk and abdominal muscles, may not have the ability to generate an effective cough. If coughing is dependent on a caregiver, these patients will cough with reduced frequency. Because the innervation to the muscles involved in cough consists of nerves that arise from varying levels of the spinal cord, some patients with spinal cord injury have partial control over these muscles and thus can cough, though with reduced efficacy. Two hundred patients with varying levels of spinal cord injury were studied to determine if motor level and cough ability are correlated. Cough efficacy was measured using a peak expiratory flowmeter while patients were seated at 90 degrees. We concluded that there is indeed a direct relationship between motor level and peak expiratory flow produced during coughing.

Adolescent↗
PubMed2003

Th1/Th2 profile in peripheral blood in atopic cough and atopic asthma.

BACKGROUND: Eosinophilic tracheobronchitis with cough hypersensitivity, abbreviated as atopic cough, is an important cause of chronic cough. The reason for the absence of airway hyper-responsiveness is unknown, differing from asthma, a Th2 cytokine-mediated disorder. OBJECTIVE: To compare the type 1 helper T cell (Th1)/Th2 balance in the peripheral blood from subjects with atopic cough and atopic asthma, we assessed the intracellular cytokine production at the single-cell level. METHODS: Thirty-six subjects (10 patients with atopic cough, 18 with atopic asthma, and eight control subjects) were included. Intracellular IL-4 and IFN-gamma were detected in CD4+ T cells by flow cytometry. RESULTS: A significantly lower ratio of IFN-gamma-/IL-4-producing CD4+ T cells after phorbol 12-myristate acetate/ionomycin stimulation was found in patients with atopic cough and atopic asthma compared with normal subjects. In comparison between atopic patients, the ratio of IFN-gamma-/IL-4-producing cells was significantly higher in atopic cough than in atopic asthma. However, the proportion of IL-4-producing CD4+ T cells was significantly higher in patients with atopic asthma than in normal control subjects and no significant difference was detected between patients with atopic cough and normal subjects. No significant difference in the proportion of IFN-gamma-producing cells was found between the subjects. Overall, the total IgE levels were positively correlated to the IL-4-producing cells and inversely correlated to the ratio of IFN-gamma-/IL-4-producing cells. CONCLUSION: These results show the lower degree of Th2 cytokine predominance in atopic cough compared with atopic asthma and suggest the relation between the Th1/Th2 balance and atopic status.

Adult↗