Analysis of the Clinical Features of Tracheobronchial Fungal Infections with Tumor-Like Lesions.

BACKGROUND: Tracheobronchial fungal infections (TBFI) cause life-threatening complications in immunocompromised hosts but are rarely reported. Misdiagnosis and delayed antifungal treatment are associated with the high mortality rate of patients with TBFI. OBJECTIVES: This study analyzed the bronchoscopic features of TBFI and their roles in the early diagnosis of TBFI. METHODS: The demographic, clinical, radiologic, and bronchoscopic data of 53 patients diagnosed with TBFI in our department during a 15-year period were retrospectively analyzed. RESULTS: Most of the TBFI patients were male, and mass was the most common radiologic abnormality. Obvious predilection in primary bronchus distributions was observed. 41.9% of the 43 Aspergillus tracheobronchitis (AT) patients, 70% of the 10 tracheobronchial mucormycosis (TM) patients, and 100% of the 3 endobronchial cryptococcosis patients had been misdiagnosed as having cancer on bronchoscopy because of the presence of tumor-like lesions. The most common features of AT were bronchial occlusion with a mass or mucosal necrosis, bronchial stenosis with mucosal hyperplasia, or uneven mucosa. The main descriptions of TM were bronchial stenosis or obstruction due to mucosal necrosis, uneven mucosa, or a mass. The endoscopic characteristics of endobronchial cryptococcosis included occlusion due to uneven mucosa or mass, or external compressive stricture. CONCLUSION: Immunocompromised patients and immunocompetent patients with underlying disease displaying tumor-like lesions on bronchoscopy should be differentially diagnosed with cancer. Bronchial biopsy is indispensable for the early diagnosis of TBFI.

Live Imaging of Influenza Infection of the Trachea Reveals Dynamic Regulation of CD8+ T Cell Motility by Antigen.

During a primary influenza infection, cytotoxic CD8+ T cells need to infiltrate the infected airways and engage virus-infected epithelial cells. The factors that regulate T cell motility in the infected airway tissue are not well known. To more precisely study T cell infiltration of the airways, we developed an experimental model system using the trachea as a site where live imaging can be performed. CD8+ T cell motility was dynamic with marked changes in motility on different days of the infection. In particular, significant changes in average cell velocity and confinement were evident on days 8-10 during which the T cells abruptly but transiently increase velocity on day 9. Experiments to distinguish whether infection itself or antigen affect motility revealed that it is antigen, not active infection per se that likely affects these changes as blockade of peptide/MHC resulted in increased velocity. These observations demonstrate that influenza tracheitis provides a robust experimental foundation to study molecular regulation of T cell motility during acute virus infection.

[The problems associated with the treatment of stenosing laryngotracheitis in the children (the results of the 35 year-long experience)]. / Problemy lecheniia stenoziruiushchego laringotrakheita u detei (rezul'taty 35-letnego opyta).

Stenosing laryngotracheitis (SLT) affecting the children is considered to be an emergency pediatric condition associated with ENT pathology. Its treatment presents a serious challenge for otolaryngologists, pediatricians, specialists in communicable diseases, allergologists, etc. We have undertaken a retrospective analysis of the available data with a view to summarizing the tendencies in the evolution of SLT morbidity. The results of the 35 year-long experience with the use of the currently available therapeutic strategies for the treatment of the children suffering from stenosing laryngotracheitis are presented. Special emphasis is laid on the advantages of the combined treatment of the patients presenting with this condition based at a specialized infectious department with the participation of an otorhinolaryngologist.

[Cytokine profile in young children with acute stenotic laryngotracheitis].

INTRODUCTION: One of the most severe complications of acute respiratory infections in young children is acute stenotic laryngotracheitis (croup). The relationship between cytokine blood levels and symptoms of croup, croup severity, disease sequel, despite numerous studies is still unclear. AIM: Cytokine profile in young children with acute stenotic laryngotracheitis investigation. MATERIAL AND METHODS: 112 children aged 12 min. - 36 mon. with acute stenotic laryngotracheitis which were treated at the Lviv Regional Infectious Diseases Hospital were kept under observation. Croup symptoms, levels of interleukins (IL1, IL4, IL6, IL10, IL17) in serum, DNA and RNA viruses in respiratory nasal mucus were studied; Chan croup severity was used. RESULTS: In the pathogenesis of croup has an important role the imbalance between inflammatory (IL1, IL6) and anti-inflammatory (IL4, IL10, IL17) cytokines, which does not reduce the intensity of inflammatory reactions and its lead to local swelling, muscle spasm, excessive production of mucus in the place of viral replication. The levels of inflammatory and anti-inflammatory cytokines in the blood serum of children with croup were significantly higher than in patients with acute laryngitis. In patients with recurrent croup, unlike patients with the first case of croup does we don't see a significant correlation between the concentrations of inflammatory and anti-inflammatory cytokine levels Conclusions: The significantly higher levels of cytokines in children with croup compared with the group of patients with acute laryngitis were found, imbalance between anti-inflammatory (IL1, IL6) cytokine levels and inflammatory (IL4, IL10, IL17) cytokine levels in children who developed recurrent croup.

[SOME CLINICAL AND CYTOKINE FEATURES OF THE CLINICAL COURSE OF RECURRENT RESPIRATORY SYSTEM DISEASES IN CHILDREN WITH THE TOXOCARIASIS INVASION].

The aim of the present study was to analyze clinical and cytokine features of recurrent respiratory system diseases in children with toxocariasis. 50 children aged 1 to 17 years (mean age - 10±5 years) with recurrent current of respiratory system disorders were studied. During the survey such clinical manifestations of the respiratory system disorders as obstructive bronchitis (50%), bronchial asthma (30%), pneumonia (10%) and laryngotracheitis (10%) have been revealed. Statistical analysis of the results was performed using the software package STATISTICA 6.1 (SNANSOFT). We have shown that the disorders of respiratory system in case of toxocariasis invasion often occur with severe intoxication and bronchial obstruction syndromes, temperature reaction, respiratory insufficiency and hepatomegaly. A prolonged course of the disease has been noted. "Inflammatory" indicators of general blood analysis, such as leukocytosis and increased of ESR have been recorded in patients with respiratory system disorders in children with T.canis infection significantly more often, significant "allergic" laboratory changes were in the form of eosinophilia. High average levels of pro-inflammatory IL-6, as well as low levels of IL 5 have been determined in children suffering from the respiratory system disorders and with toxocariasis invasion in the anamnesis. The obtained findings require further study.

Distinct patterns of leukocyte recruitment in the pulmonary microvasculature in response to local and systemic inflammation.

The mechanisms of leukocyte recruitment in the pulmonary microvasculature in response to local and systemic inflammation remain elusive. Male C57BL/6 mice received lipopolysaccharide (LPS) intrapulmonary (intratracheally, it) or systemically (intravenously, iv) for 1-18 h. Leukocyte responses in lung were analyzed by use of intravital fluorescence microscopy. Plasma and lung levels of CXC chemokines as well as Mac-1 and F-actin expression in leukocytes and bronchoalveolar leukocytes were quantified. Venular leukocyte rolling was markedly increased in response to local LPS but only marginally after systemic LPS. Leukocyte adhesion in venules was enhanced in both groups although adhesion was higher in mice receiving LPS intratracheally compared with LPS intravenously. Systemic LPS caused more leukocytes trapping in capillaries compared with local LPS. The ratio of adherent leukocytes in venules compared with capillaries was higher in response to local LPS, suggesting that leukocytes were more prone to accumulate in venules in local inflammation and in capillaries in systemic inflammation. Systemic LPS triggered higher F-actin formation and Mac-1 expression in leukocytes compared with local LPS. Local and systemic LPS caused similar increases in CXC chemokines in the lung whereas intravenous endotoxin provoked higher levels of CXC chemokines in the circulation. Interestingly, intratracheal LPS increased recruitment of leukocytes in the alveolar space whereas intravenous LPS was ineffective in promoting leukocyte accumulation in the bronchoalveolar space. In conclusion, our data demonstrate that pulmonary microvascular recruitment of leukocytes differs in local and systemic inflammation, which might be related to premature activation and stiffening of circulating leukocytes in endotoxemia.

Tracheobronchial mycosis in a retrospective case-series study of five status asthmaticus patients.

The etiology of status asthmaticus (SA), a complication of severe asthma, is unknown. Fungal exposure, as measured by fungal atopy, is a major risk factor for developing asthma, but the relationship of fungi in SA per se has not previously been reported. In this five patient retrospective case series study, lower respiratory tract cultures were performed on bronchoalveolar lavage or tracheal aspirate fluid, comparing standard clinical laboratory cultures with a specialized technique in which respiratory mucus was removed prior to culture. We show that mucolytic treatment allows an increased detection of fungal growth, especially yeast, from the lower airways of all SA patients. We also demonstrate that inhalation of the yeast Candida albicans readily induces asthma-like disease in mice. Our observations suggest that SA may represent a fungal infectious process, and support additional prospective studies utilizing anti-fungal therapy to supplement conventional therapy, broad-spectrum antibiotics and high-dose glucocorticoids, which can promote fungal overgrowth.

Acute intratracheal Pseudomonas aeruginosa infection in cystic fibrosis mice is age-independent.

BACKGROUND: Since the discovery of the human CFTR gene in 1989 various mouse models for cystic fibrosis (CF) have been generated and used as a very suitable and popular tool to approach research on this life-threatening disease. Age related changes regarding the course of disease and susceptibility towards pulmonary infections have been discussed in numerous studies. METHODS: Here, we investigated CftrTgH(neoim)Hgu and Cftrtm1Unc-Tg(FABPCFTR)1Jaw/J CF mice and their non-CF littermates during an acute lung infection with Pseudomonas aeruginosa for age dependent effects of their lung function and immune response.Mice younger than three or older than six months were intratracheally infected with P. aeruginosa TBCF10839. The infection was monitored by lung function of the animals using non-invasive head-out spirometry and the time course of physiological parameters over 192 hours. Quantitative bacteriology and lung histopathology of a subgroup of animals were used as endpoint parameters. RESULTS: Age-dependent changes in lung function and characteristic features for CF like a shallower, faster breathing pattern were observed in both CF mouse models in uninfected state. In contrast infected CF mice did not significantly differ from their non-CF littermates in susceptibility and severity of lung infection in both mouse models and age groups. The transgenic Cftrtm1Unc-Tg(FABPCFTR)1Jaw/J and their non-CF littermates showed a milder course of infection than the CftrTgH(neoim)Hgu CF and their congenic C57Bl/6J non-CF mice suggesting that the genetic background was more important for outcome than Cftr dysfunction. CONCLUSIONS: Previous investigations of the same mouse lines have shown a higher airway susceptibility of older CF mice to intranasally applied P. aeruginosa. The different outcome of intranasal and intratracheal instillation of bacteria implies that infected CF epithelium is impaired during the initial colonization of upper airways, but not in the subsequent response of host defense.

Overexpression of HO-1 protects against TNF-alpha-mediated airway inflammation by down-regulation of TNFR1-dependent oxidative stress.

Oxidative stresses are believed to play an important role in the induction of both cell adhesion molecules and pro-inflammatory cytokines, a key event in a variety of inflammatory processes. The enzyme heme oxygenase-1 (HO-1) functions as an antioxidant and serves to protect against tissue injury. In this study, we report that HO-1 was induced in cultured human tracheal smooth muscle cells after either treatment with a potent inducer of HO-1 activity, cobalt protoporphyrin IX, or infection with a recombinant adenovirus that carries the human HO-1 gene. Overexpression of HO-1 protected against tumor necrosis factor (TNF)-alpha-mediated airway inflammation via the down-regulation of oxidative stress, adhesion molecules, and interleukin-6 in both cultured human tracheal smooth muscle cells and the airways of mice. In addition, HO-1 overexpression inhibited TNF-alpha-induced intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 expression, adherence of THP-1 cells, generation of interleukin-6, p47(phox) translocation, and nuclear factor-kappaB activation. HO-1 overexpression also attenuated TNF-alpha-induced oxidative stress, which was abrogated in the presence of both the HO-1 inhibitor, zinc protoporphyrin IX, as well as a carbon monoxide scavenger. In addition, HO-1 overexpression reduced the formation of a TNFR1/c-Src/p47(phox) complex. These results suggest that HO-1 functions as a suppressor of TNF-alpha signaling, not only by inhibiting the expression of adhesion molecules and generation of interleukin-6, but also by diminishing intracellular reactive oxygen species production and nuclear factor-kappaB activation in both cultured human tracheal smooth muscle cells and the airways of mice.

Hydrogen sulfide exposure triggers chicken trachea inflammatory injury through oxidative stress-mediated FOS/IL8 signaling.

Hydrogen sulfide (H2S) is well known to cause irritation and damage to airway following inhalation, but the mechanism by which H2S contributes to airway toxicity is unclear. In order to assess the respiratory toxicity of H2S inhalation in chicken trachea, we investigated the change of oxidative stress parameters, tracheal tissue structure and transcriptome profiles of chicken trachea exposed to H2S for 42 days. The results showed H2S exposure induced oxidative stress and inflammation in trachea. The ultrastructural analysis revealed loss of cilia and accumulation of mucus in tracheal epithelium. Differentially expressed genes (DEGs) analysis indicated 454 genes were significantly changed, including 136 genes upregulated and 318 genes downregulated. Gene ontology and KEGG analysis showed many genes involved in response to oxidative stress, inflammatory and immune response, which might contribute to H2S-induced tracheal inflammatory injury. Among those genes, N-acetyl-L-cysteine (NAC) treatment blocked the H2S-triggered expression of FOS and IL8. Silencing FOS by siRNA inhibited H2S-induced expression of IL8. Taken together, we concluded that H2S induced oxidative stress leads to tracheal inflammation through FOS/IL8 signaling, leading to excessive mucus secretion and absence of cilia. These results provide new insights for unveiling the biological effects of H2S in vivo and in vitro.

[Suppression effect of different stage antigens of Schistosoma japonicum on airway inflammation in a murine model of asthma].

OBJECTIVE: To investigate the effect of antigens of different stage Schistosoma japonicum on airway inflammation in a murine model of asthma. METHODS: 48 female BALB/c mice were randomly divided into eight groups. Mice in group A were given normal saline of equal volume as control. Group B was asthma model which was established by intraperitoneal and intranasal challenge with OVA. Mice in groups C, D and E were immunized with soluble egg antigen (SEA), soluble male worm antigen (SWA), and schistosomulum antigen (SSA) respectively 4 times in a week interval, followed by OVA sensitization as in group B 1 week after the final immunization. Mice in groups F, G, and H were immunized with SEA, SWA, and SSA respectively but sensitized and challenged with saline instead of OVA. 48 hours after asthma was induced, the mice were sacrificed. Leukocytes and eosinophils were counted in bronchoalveolar lavage fluid (BALF). The level of IL-5, IL-10 and IFN-gamma in BALF was detected. Pathologic changes in lung tissues were observed. RESULTS: Inflammation cells, especially eosinophils, appeared in airways of mice in groups B, C, D and E, but with much less number in groups C, D and E. No inflammation cells were seen in airways of group A mice. The number of leukocytes, eosinophils and level of IL-5 in BALF of group B [(98.4 +/- 16.1) x 10(4)/ml, (17.6 +/- 4.3) x 10(4)/ml, (197.9 +/- 36.5) pg/ml respectively] were significantly higher than those of group A [(8.2 +/- 1.1) x 10(4)/ml, (0.02 +/- 0.01) x 10(4)/ ml, (12.3 +/- 7.4) pg/ml], however the levels of IL-10 and IFN-gamma were significantly lower than that of group A (P < 0.05). The number of leukocytes, especially eosinophils, in BALF of groups C, D and E was significantly lower than that of group B. The level of IL-5 in BALF of groups C, D and E was significantly reduced, while that of IL-10 and IFN-gamma in BALF of the 3 groups was significantly higher than group B (P < 0.05). CONCLUSIONS: The immunization with S. japonicum antigens can effectively modulate the level of cytokines and inhibit the eosinophil infiltration and airway inflammation in asthmatic mice.

Autoimmune Tracheal Cartilage Inflammation Responsive to Anti-TNF-α Therapy.

Tracheal inflammation, or tracheitis, is a pathologic process that can occur secondary to a number of systemic inflammatory diseases, or it may be idiopathic in nature. Regardless of the underlying etiology, tracheitis can, in its most severe form, be life-threatening, thus making its treatment an area of interest. Our case is one of a 50-year-old man with a remote history of inflammatory bowel disease achieving clinical cure following surgical resection who presented with progressive dyspnea due to tracheal stenosis that was presumed secondary to an autoimmune and inflammatory etiology. His disease was initially refractory to recurrent surgical interventions. He ultimately achieved clinical improvement with a combination of methotrexate and the tumor necrosis factor alpha (TNF-α) inhibitor, adalimumab. While both clinical trials and standardized treatment guidelines are lacking in this domain, this case illustrates a potential role for TNF-α inhibitors in the treatment of inflammatory tracheitis, irrespective of the underlying etiology.

[Lymphocyte subsets in patients with recurrent upper airway infections]. / Limfocitu populiaciju pokyciai sergant pasikartojanciomis virsutiniu kvepavimo taku infekcinemis ligomis.

UNLABELLED: The aim of our study was to evaluate the digressions of lymphocyte subsets in patients with recurrent upper airway infectious diseases. METHODS: We studied 35 patients (mean of age 11.1+/-2.1 years) with recurrent upper airway infections. The first group consisted of patients, who had acute upper airway infections: rhinitis, pharyngitis, laryngitis and tracheitis more than 6 times per last year, sinusitis or otitis more than 4 times per last year. The control group comprised of 9 healthy subjects. Subsets of lymphocytes (CD3+, CD4+, CD8+, CD4+/CD8+, CD16+/56+ and CD19+) were detected by FACS Calibur cytometer. RESULTS: We found a significantly lower count of CD4+ lymphocytes in the patients' group compared to the control group (37.5+/-1.2 vs 45.7+/-3.1% of total lymphocytes, p<0.01). We did not find any significant differences of other lymphocyte subsets between patients and control groups. CONCLUSION: We propose that patients with recurrent upper airway infections have alterations of the cellular immunity -- decreased amount of CD4+ lymphocytes.

Antibody response to P-protein in patients with Branhamella catarrhalis infections.

Branhamella catarrhalis is now recognized as an important cause of lower respiratory tract infections, especially in the elderly. In most instances, pathogenicity is presumed by recovery of the organism in a sputum culture, a method that is less than conclusive. In order to better diagnose B. catarrhalis infections, an enzyme-linked immunoassay has been developed using P-protein as antigen to measure antibodies to B. catarrhalis. In 17 elderly patients with B. catarrhalis pneumonia and 12 with tracheobronchitis, acute-phase serum antibody titers to P-protein were found to be significantly increased when compared with those of normal subjects (both p less than 0.02). There were no differences in antibody titers between patients with pneumonia and tracheobronchitis. Antibody titers of convalescent-phase sera increased over those of acute-phase sera in 46 percent of pneumonia patients and 50 percent of tracheobronchitis patients. The results demonstrated that lower respiratory tract infections with B. catarrhalis promote a significant elevation in antibody response to P-protein of B. catarrhalis.

Acute laryngotracheitis in the rat induced by Sendai virus: the influx of six different types of immunocompetent cells into the laryngeal mucosa differs strongly between the subglottic and the glottic compartment.

OBJECTIVES: Acute laryngotracheitis is a disease in which mainly the subglottic area is infected, whereas adjacent parts of the larynx, especially the narrow glottic fold, remain unaffected. The reason for the difference between these two directly adjacent regions is unknown. Therefore, in the present study the influx of dendritic cells, neutrophils, T and B lymphocytes, natural killer cells, and macrophages into the mucosa of different laryngeal compartments was investigated after Sendai virus infection in the rat. The aims were to study both the influx of immunocompetent cells and the adhesion of the pathogen and to correlate them to the different reactions of the laryngeal areas during pseudocroup. METHODS: Acute laryngotracheitis was induced by intranasal application of Sendai virus in brown Norway rats. This virus is exclusively pneumotropic in rodents and belongs to the parainfluenza virus type 1, the main pathogen of acute laryngotracheitis in children. The numbers of dendritic cells, neutrophils, T and B lymphocytes, natural killer cells, and macrophages were determined in the supraglottic, glottic, subglottic, and tracheal mucosa on days 2, 5, 7, and 14 after virus application. Furthermore, the nucleoprotein of the virus and major histocompatibility complex (MHC) Class II expression were detected immunohistologically on the laryngeal epithelium. RESULTS: All cell subsets entered the laryngeal mucosa during inflammation. The highest influx was detected among dendritic cells subglottically. This was accompanied by a strong virus adhesion and MHC Class II expression on the subglottic epithelium. In contrast, only a few immunocompetent cells entered the adjacent glottic mucosa, and on the glottic epithelium staining for virus nucleoprotein and MHC Class II expression was weak. CONCLUSIONS: The inflammatory response of the laryngeal mucosa shows great regional differences in this animal model during experimental viral infection. The response was characterized by a strong subglottic and a weak glottic reaction. A possible reason for this difference might be region-specific viral adhesion on the epithelium of the laryngeal areas, as well as differences in MHC Class II expression. Thus, these data agree with the clinical observation during acute laryngotracheitis and may explain why the subglottic part of the larynx is affected preferentially during pseudocroup. The molecular mechanisms mediating the different reactions await clarification.

Rhinotracheitis in turkey poults.

A severe upper respiratory disease of young turkeys is described that resulted in high morbidity and mortality. Death was due to asphyxiation produced by occlusion of the trachea or nostrils. The postmortem lesions were tracheitis, pulmonary edema, swollen livers and spleens, and a drastic reduction in bursa size. Bursal necrosis and loss of tracheal epithelium were found in tissue sections from clinically affected birds. Antibody to infectious bursal disease was found by agar-gel precipitin and virus-neutralization tests of serum samples from affected flocks. A geometric mean titer of 31.5 for Newcastle disease was found in unvaccinated flocks of five-week-old turkeys.

Respiratory disease (rhinotracheitis) of turkeys in Brittany, France. III. Interaction of multiple infecting agents.

A candidate breeder flock of turkeys was studied during and after an outbreak of rhinotracheitis. Laboratory studies revealed the presence of three pathogens during the acute phase of the disease. These agents were hemorrhagic enteritis virus (HEV), paramyxovirus type 2 (PMV2), and chlamydia. Twenty-five turkeys in the flock were individually identified, and blood samples from these birds were collected for serological studies each week for 21 weeks. The serological results revealed high titers for HEV and chlamydia but very low titers for PMV2.

Respiratory disease (rhinotracheitis) in turkeys in Brittany, France, 1981-1982. I. Field observations and serology.

During the summer of 1981, a respiratory disease epidemic occurred in turkeys in Brittany, France. Since this initial epizootic, which lasted through fall, epizootic waves similar to the initial one have occurred at approximately 6-month intervals, with smaller peaks at 2-month intervals. The epidemiology, clinical signs, and postmortem findings were highly suggestive of an epizootic of chlamydiosis. Serological tests for chlamydia, paramyxoviruses, avian influenza, adenovirus 127, mycoplasma, and Alcaligenes faecalis were conducted. The chlamydia tests were the only ones consistently positive.

Dendritic cell influx differs between the subglottic and glottic mucosae during acute laryngotracheitis induced by a broad spectrum of stimuli.

Clinically, the subglottic and glottic mucosae may react differently, eg, during acute laryngotracheitis. In healthy rats, we showed previously that the composition of the mucosal immune system of the larynx also differs between these areas. Neutrophils, lymphocytes, and dendritic cells (DCs) are part of this mucosal immune system. In particular, DCs occupy a key function. They migrate into inflamed mucosae during the early phase of the immune response, which is normally characterized by an influx of neutrophils. Thus, they help to overcome the time lag between the innate and the adaptive immune responses. In the present study, the influx of DCs, neutrophils, and T lymphocytes into the subglottic and glottic mucosae of rats was examined at different time points after challenge with a broad spectrum of stimuli such as dead Moraxella catarrhalis, viable Bordetella pertussis, viable Sendai virus, and the soluble protein ovalbumin. The number of DCs increased rapidly after the application of the antigens. This increase was as rapid as the increase in neutrophils. Depending on the kind of antigen, their number in the mucosa increased up to 1,000 cells per 0.1 mm2 (Sendai virus). The comparison of different mucosal areas shows that an overwhelming number of immunocompetent cells entered the subglottic mucosa, whereas only a few cells migrated into the adjacent glottic mucosa. In conclusion, after inhalation of different kinds of antigens, the subset of immunocompetent cells investigated in this study entered the laryngeal mucosa in high numbers. The number of DCs entering the laryngeal mucosa was higher than the numbers of the other immune cells investigated. This finding underlines their function as first-line sentinels of the mucosal immune system of the larynx. The observation that the number of cells entering the laryngeal mucosa is location-dependent indicates the ability of adjacent laryngeal regions to react differently. This is similar to the clinical observation of a selective subglottic reaction during acute laryngotracheitis.

[Interleukin-8 and airway inflammation].

Airway inflammation is a prominent feature of chronic obstructive diseases of the airways, including asthma, bronchiectasis, chronic bronchitis, and diffuse panbronchiolitis. Neutrophils are implicated in the pathogenesis of these diseases. The present review discusses the role of interleukin-8 (IL-8), a neutrophil chemo-attractant, in neutrophil accumulation in the airways, and the mechanisms of inducing IL-8 expression. IL-8 presents in the sputum of patients with inflammatory airway diseases, and accounts in large part for the chemo-attractant activity present. Focusing on Pseudomonas aeruginosa as the stimulus, it was discovered that when a supernatant of bacterial culture is introduced into the airways in vivo, bacterial products induce IL-8 expression in surface airway epithelial cells and the recruitment of neutrophils into the airways. The neutrophil chemotactic activity of the airway fluid was inhibited by an IL-8 antibody. The luminal IL-8 concentration increased in response to instillation of bacteria, and an inhibitor of neutrophil recruitment markedly reduced the IL-8 levels. From these results, it was speculated that bacteria-induced neutrophil accumulation in the airways involves a cascade of events, and that early neutrophil recruitment in response to bacteria is due to epithelium-derived IL-8, while the amplification of the response is due, at least in part, to IL-8 induction in the neutrophils themselves.