Nasal Mucosa
Respiratory Mucosa
Mucous Membrane
Olfactory Mucosa
Mucociliary Clearance
Respiratory System
Microscopy, Electron, Scanning
Bacterial Adhesion
Haemophilus influenzae
Organ Culture Techniques
Intestinal Mucosa
Gastric Mucosa
Mouth Mucosa
Colon
Laryngeal Mucosa
Duodenum
Intestine, Small
Stomach Ulcer
Effects of inhaled beta agonist and corticosteroid treatment on nuclear transcription factors in bronchial mucosa in asthma. (1/2809)
BACKGROUND: Inhaled corticosteroids and beta agonists are the most commonly used treatments in asthma and are often used together. Recent evidence suggests that many of the anti-inflammatory actions of corticosteroids are mediated by cross-talk between the activated glucocorticoid receptor (GR) and other transcription factors such as the pro-inflammatory nuclear factor kappa B (NFkappaB). Beta agonists can activate the transcription factor cAMP response element binding protein (CREB). A mutual inhibition between GR and CREB occurs in vitro which raises the possibility of a negative interaction between corticosteroid and beta agonist drugs. A study was undertaken to determine whether these interactions occur during treatment with beta2 agonists and corticosteroids in asthma. METHODS: Seven subjects who were participating in a randomised, placebo controlled, crossover study of six weeks treatment with inhaled budesonide (400 microg twice daily), terbutaline (1 mg four times daily), and combined treatment were recruited. Biopsy samples of the bronchial mucosa were obtained after each treatment and analysed for the DNA binding activity of GR, CREB, and NFkappaB. RESULTS: Budesonide increased GR activity (p<0.05) and decreased NFkappaB activity (p<0.05). No treatment combination altered CREB activity and terbutaline had no significant effects on any transcription factor. CONCLUSIONS: Inhaled corticosteroids have significant effects on GR and NFkappaB activity in bronchial mucosa. A negative interaction between inhaled corticosteroids and beta agonists was not found. (+info)Passive IgA monoclonal antibody is no more effective than IgG at protecting mice from mucosal challenge with respiratory syncytial virus. (2/2809)
Respiratory syncytial virus (RSV) is a mucosally restricted pathogen that can cause severe respiratory disease. Although parenteral administration of sufficient RSV-specific IgG can reduce severity of lower respiratory tract infection in high-risk infants, delivery of antibody by direct airway administration is an attractive alternative. Topical and parenteral administration of an IgA monoclonal antibody (MAb) specific for the RSV F glycoprotein was compared with an IgG MAb, specific for the same antigenic site, for ability to protect mice against RSV infection. Administration of RSV-specific IgG was more effective in reducing RSV titers in lung (4.6 log10 pfu/g) than IgA MAb (3.6 log10 pfu/g) when given intranasally immediately prior to infection (P=.005). RSV titers in the nose were reduced only by prophylactic administration of IgG parenterally. Therefore, topical administration of IgA is no more effective than topically administered IgG and is less effective than systemically administered IgG for protecting against RSV infection. (+info)Differential sensitivity of normal and cystic fibrosis airway epithelial cells to epinephrine. (3/2809)
1. Exposure to epinephrine has been shown to have a range of effects on cells and tissues. A recent study suggested that the proliferative ability of CF epithelial cells, exposed to high concentrations of epinephrine (200 - 300 microM), was reduced when compared to that of normal cells. This approach could potentially provide a means to effectively separate cells with functional cyclic AMP-dependent Cl-ion transport from those defective in this pathway. 2. The sensitivity to killing by epinephrine is reported here for four different CF cell lines, three normal cell lines, and two CF epithelial cell lines complemented with wild-type (wt) CF transmembrane conductance regulator (CFTR) cDNA. 3. While each cell line exhibited varying sensitivity to 200 microM epinephrine, no predictable pattern was observed between the expression of wt-CFTR and cell survival following epinephrine exposure. Overall, normal cell lines did exhibit a greater resistance to epinephrine-induced cell death although, the most resistant cell line was derived from CF tracheal epithelium (SigmaCFTE29o-). 4. The expression of exogenous wt-CFTR increased the survival of one cell line (CFDEo-) when compared to the parent line, but in another complemented line, survival was reduced. 5. These findings suggest that while epinephrine induces cell killing, it is not consistently effective for preferential selection of normal over CF cells. Although CFTR may play a role in the mechanism(s) of epinephrine killing, other factors such as cell density, proliferative ability, cell type origin and phenotype are involved. (+info)Crucial role of the interleukin 1 receptor family member T1/ST2 in T helper cell type 2-mediated lung mucosal immune responses. (4/2809)
T1/ST2 is an orphan receptor of unknown function that is expressed on the surface of murine T helper cell type 2 (Th2), but not Th1 effector cells. In vitro blockade of T1/ST2 signaling with an immunoglobulin (Ig) fusion protein suppresses both differentiation to and activation of Th2, but not Th1 effector populations. In a nascent Th2-dominated response, anti-T1/ST2 monoclonal antibody (mAb) inhibited eosinophil infiltration, interleukin 5 secretion, and IgE production. To determine if these effects were mediated by a direct effect on Th2 cells, we next used a murine adoptive transfer model of Th1- and Th2-mediated lung mucosal immune responses. Administration of either T1/ST2 mAb or T1/ST2-Ig abrogated Th2 cytokine production in vivo and the induction of an eosinophilic inflammatory response, but failed to modify Th1-mediated inflammation. Taken together, our data demonstrate an important role of T1/ST2 in Th2-mediated inflammatory responses and suggest that T1/ST2 may prove to be a novel target for the selective suppression of Th2 immune responses. (+info)Epithelial P2X purinergic receptor channel expression and function. (5/2809)
P2X purinergic receptor (P2XR) channels bind ATP and mediate Ca(2+) influx--2 signals that stimulate secretory Cl(-) transport across epithelia. We tested the hypotheses that P2XR channels are expressed by epithelia and that P2XRs transduce extracellular ATP signals into stimulation of Cl(-) transport across epithelia. Electrophysiological data and mRNA analysis of human and mouse pulmonary epithelia and other epithelial cells indicate that multiple P2XRs are broadly expressed in these tissues and that they are active on both apical and basolateral surfaces. Because P2X-selective agonists bind multiple P2XR subtypes, and because P2X agonists stimulate Cl(-) transport across nasal mucosa of cystic fibrosis (CF) patients as well as across non-CF nasal mucosa, P2XRs may provide novel targets for extracellular nucleotide therapy of CF. (+info)Effect of fluticasone propionate and salmeterol on Pseudomonas aeruginosa infection of the respiratory mucosa in vitro. (6/2809)
The purpose of this study was to investigate the effect of the corticosteroid, fluticasone propionate (FP), on Pseudomonas aeruginosa infection of the respiratory mucosa of an organ culture model in vitro. Organ cultures infected with P. aeruginosa had significantly (p< or =0.05) elevated levels of mucosal damage and significantly (p< or =0.05) less ciliated cells compared to controls. Preincubation of tissue with FP (10(-6) or 10(-5) but not 10(-7) M) prior to P. aeruginosa infection significantly (p< or =0.05) reduced the bacterially induced mucosal damage in a concentration-dependent manner. FP (10(-5) M) also significantly (p< or =0.05) prevented loss of ciliated cells. FP did not alter the density of bacteria adherent to the different mucosal features of the organ cultures, but did reduce total bacterial numbers due to the reduced amount of damaged tissue, which is a preferred site of P. aeruginosa adherence. It has previously been shown that the long-acting beta2-agonist salmeterol (4 x 10(-7)M) also reduces the mucosal damage caused by P. aeruginosa infection, probably via elevation of intracellular cyclic adenosine monophosphate concentrations. Preincubation of tissue with both 10(-7)M FP and 10(-7)M salmeterol, concentrations at which they did not by themselves influence the effect of P. aeruginosa infection, significantly (p< or =0.05) reduced P. aeruginosa-induced loss of cilia. However, there was no additional benefit from adding 4 x 10(-7)M salmeterol to 10(-6)M FP. In conclusion fluticasone propionate reduced mucosal damage caused by P. aeruginosa infection in vitro and preserved ciliated cells. There was a synergistic action with salmeterol in the preservation of ciliated cells. (+info)M1/MUC5AC mucin released by human airways in vitro. (7/2809)
A series of monoclonal antibodies which bind to a mucin known as M1 (anti-M1 MAbs) have also been shown to detect the product of the human gene MUC5AC. The aim of this investigation was to determine the concentration of the M1 mucin in the surface epithelium of human bronchial preparations by means of immunohistochemistry and in the bronchial fluid derived from human airways by means of an immunoradiometric assay. Human bronchial ring preparations from the resection material of 20 patients were challenged with methacholine, leukotriene D4, or anti-immunoglobulin E. Experiments were performed in preparations with an intact epithelium as well as in tissues in which the epithelium had been mechanically removed. The anti-M1 MAbs stained the goblet cells in the epithelium intensely and there was also light and less uniform staining in the submucosa. The M1/MUC5AC mucin in the fluids secreted by the bronchial preparations was not modified during either the experimental protocol or stimulation with the different secretagogues. However, in preparations in which the epithelium had been removed, there was a significant reduction in the amount of M1/MUC5AC mucin detected. These data suggest that the M1/MUC5AC mucin detected in the biological fluids produced by human airways in vitro may be released constantly, and principally from the goblet cells in the epithelial layer. (+info)Arsenite exposure of cultured airway epithelial cells activates kappaB-dependent interleukin-8 gene expression in the absence of nuclear factor-kappaB nuclear translocation. (8/2809)
Airway epithelial cells respond to certain environmental stresses by mounting a proinflammatory response, which is characterized by enhanced synthesis and release of the neutrophil chemotactic and activating factor interleukin-8 (IL-8). IL-8 expression is regulated at the transcriptional level in part by the transcription factor nuclear factor (NF)-kappaB. We compared intracellular signaling mediating IL-8 gene expression in bronchial epithelial cells cultured in vitro and exposed to two inducers of cellular stress, sodium arsenite (As(III)), and vanadyl sulfate (V(IV)). Unstimulated bronchial epithelial cells expressed IL-8, and exposure to both metal compounds significantly enhanced IL-8 expression. Overexpression of a dominant negative inhibitor of NF-kappaB depressed both basal and metal-induced IL-8 expression. Low levels of nuclear NF-kappaB were constitutively present in unstimulated cultures. These levels were augmented by exposure to V(IV), but not As(III). Accordingly, V(IV) induced IkappaBalpha breakdown and NF-kappaB nuclear translocation, whereas As(III) did not. However, both As(III) and V(IV) enhanced kappaB-dependent transcription. In addition, As(III) activation of an IL-8 promoter-reporter construct was partially kappaB-dependent. These data suggested that As(III) enhanced IL-8 gene transcription independently of IkappaB breakdown and nuclear translocation of NF-kappaB in part by enhancing transcription mediated by low levels of constitutive nuclear NF-kappaB. (+info)Symptoms of gastritis may include abdominal pain, nausea, vomiting, loss of appetite, and difficulty swallowing. In severe cases, bleeding may occur in the stomach and black tarry stools may be present.
Diagnosis of gastritis is typically made through endoscopy, during which a flexible tube with a camera and light on the end is inserted through the mouth to visualize the inside of the stomach. Biopsies may also be taken during this procedure to examine the stomach tissue under a microscope for signs of inflammation or infection.
Treatment of gastritis depends on the underlying cause, but may include antibiotics for bacterial infections, anti-inflammatory medications, and lifestyle modifications such as avoiding alcohol, losing weight, and eating smaller more frequent meals. In severe cases, surgery may be necessary to remove damaged tissue or repair any ulcers that have developed.
Stomach ulcers are caused by an imbalance between the acid and mucus in the stomach, which can lead to inflammation and damage to the stomach lining. Factors that can contribute to the development of a stomach ulcer include:
* Infection with the bacterium Helicobacter pylori (H. pylori)
* Overuse of nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, and naproxen
* Excessive alcohol consumption
* Smoking
* Stress
* Zollinger-Ellison syndrome, a rare condition that causes the stomach to produce too much acid.
Symptoms of a stomach ulcer may include:
* Pain in the upper abdomen, often described as a burning or gnawing sensation
* Nausea and vomiting
* Bloating and gas
* Abdominal tenderness
* Loss of appetite
* Weight loss
Treatment for stomach ulcers typically involves antibiotics to kill H. pylori, if present, and acid-suppressing medications to reduce the amount of acid in the stomach. In severe cases, surgery may be necessary. Lifestyle changes, such as avoiding NSAIDs, alcohol, and smoking, can also help manage symptoms and prevent recurrence.
Preventive measures for stomach ulcers include:
* Avoiding NSAIDs and other irritating substances
* Using acid-suppressing medications as needed
* Maintaining a healthy diet and lifestyle
* Managing stress
* Avoiding excessive alcohol consumption
It is important to seek medical attention if symptoms persist or worsen over time, as stomach ulcers can lead to complications such as bleeding, perforation, and obstruction. Early diagnosis and treatment can help prevent these complications and improve outcomes.
Nasal mucosa
Respiratory epithelium
Respiratory tract
Angioedema
TST (gene)
Bordetella avium
Corynebacterium diphtheriae
Interleukin 16
Benzalkonium chloride
Corex
Respiratory system of the horse
Composition of electronic cigarette aerosol
Surgical humidification
Nasal glands
Oxygen therapy
Human nose
Influenza A virus subtype H3N8
Bovine alphaherpesvirus 5
Micrococcus luteus
Ancylostoma braziliense
Herpes simplex research
Urbach-Wiethe disease
Maleic anhydride
Mucociliary clearance
Mycoplasma pneumonia
Nasal concha
Linguatulosis
Anaphylaxis
Feline coronavirus
Sarocladium kiliense
Zinc deficiency
Trimeric autotransporter adhesin
Tonsil
Dental trauma
Histophilus somni
Halostachine
Low-grade myofibroblastic sarcoma
Xerostomia
Dead space (physiology)
Acute inhalation injury
Olfactory system
Eikenella corrodens
Gastric bypass surgery
Pulmonary alveolus
Influenza
Tobacco smoking
Salivary gland disease
Oral manifestations of systemic disease
Peyer's patch
Cysteinyl leukotriene receptor 1
Radiation therapy
List of skin conditions
Plasma cell
Outline of the human brain
Mass vaccination
Mucin 4
Duck plague
A human airway mucosa tissue model to investigate whooping cough | European Respiratory Society
Immunolocalization of aquaporins 1, 3, and 5 in the nasal respiratory mucosa of a panting species, the sheep (Ovis aries). | J...
Table - Postmortem Stability of SARS-CoV-2 in Nasopharyngeal Mucosa - Volume 27, Number 1-January 2021 - Emerging Infectious...
Details for:
Bacterial infections of respiratory and gastrointestinal mucosae :
› WHO HQ Library catalog
TGF-beta1 induces human alveolar epithelial to mesenchymal cell transition (EMT)
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Upper Respiratory Tract Infection: Practice Essentials, Background, Pathophysiology
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Pathology of diacetyl and 2,3-pentanedione airway lesions in a rat model of obliterative bronchiolitis - PubMed
RFA-AI-08-020: Immune Defense Mechanisms at the Mucosa (R21)
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Pediatric Pneumonia: Practice Essentials, Background, Pathophysiology
Nasal16
- Immunolocalization of aquaporins 1, 3, and 5 in the nasal respiratory mucosa of a panting species, the sheep (Ovis aries). (bvsalud.org)
- The nasal respiratory mucosa is the primary site for evaporative water loss in panting species, necessitating the movement of water across the nasal epithelium . (bvsalud.org)
- Whether the requirement for enhanced capacity for transepithelial water movement in the nasal respiratory mucosa of panting species has led to differences in AQP localization is unknown. (bvsalud.org)
- Using immunohistochemistry , we report the localization of AQP1, 3, and 5 in the nasal respiratory mucosa of sheep being exposed to ambient temperatures of ~21 °C or ~38 °C for 4.5 h before death (n=3/ treatment ). (bvsalud.org)
- The distribution and co- localization of AQPs in the ovine nasal respiratory mucosa is different to that reported in non-panting species and may reflect the physiological demands associated with enhanced respiratory evaporation . (bvsalud.org)
- We propose that AQP1, 3, and 5 may constitute a transepithelial water pathway via glandular secretions and across the surface epithelium , which provides a possible means for rapid and controllable water movement in the nasal respiratory mucosa of a panting species. (bvsalud.org)
- 5. Distribution of respiratory mucin proteins in human nasal mucosa. (nih.gov)
- These include very short incubation periods, rapid host-to-host transmission and replication in the nasal mucosa rather than throughout the body. (nih.gov)
- Medical examination revealed slight irritation of the nasal mucosa in only one worker. (cdc.gov)
- Very valuable in cases of rhinitis, inflammation of nasal mucosa, septal erosion, and other disorders of respiratory pathways. (slideshare.net)
- Jaspers' data shows that smoking cigarettes causes suppression of several key immune genes in the nasal mucosa. (eurekalert.org)
- The disease is caused by Avibacterium paragallinarum, which inflicts initial damage to the nasal and respiratory epithelium. (usda.gov)
- In the present study, we created three-dimensional tissue models of the human ciliated nasal and tracheo-bronchial mucosa. (uni-wuerzburg.de)
- Applying molecular biological, histological, and microbiological assays, we found that 1 µg/ml CyaA elevated the intracellular cAMP level but did not disturb the epithelial barrier integrity of nasal and tracheo-bronchial airway mucosa tissue models. (uni-wuerzburg.de)
- Even though the nasal and the tracheo-bronchial mucosa appear similar from a histological perspective, they are differentially susceptible to B. pertussis CyaA in vitro. (uni-wuerzburg.de)
- Our finding that nasal tissue models showed an increased innate immune response towards the B. pertussis virulence factor CyaA compared to tracheo-bronchial tissue models may reflect the key role of the nasal airway mucosa as the first line of defense against airborne pathogens. (uni-wuerzburg.de)
Epithelial Cells1
- Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viral entry factors such as ACE2 and TMPRSS members were broadly enriched in epithelial cells of the glands and oral mucosae. (nature.com)
Tract15
- Sulfur mustard may cause cancer in the On dry surface soil, volatilization would respiratory tract and skin of humans. (cdc.gov)
- Upper respiratory tract infection (URI) represents the most common acute illness evaluated in the outpatient setting. (medscape.com)
- Details of the patient's history aid in differentiating a common cold from conditions that require targeted therapy, such as group A streptococcal pharyngitis , bacterial sinusitis, and lower respiratory tract infections. (medscape.com)
- Gasoline is not as readily absorbed from the gastrointestinal tract as from the respiratory tract. (cdc.gov)
- It affects the skin, the peripheral nerves, the mucosa of the upper respiratory tract, and the eyes. (who.int)
- A more recent article on antibiotic use in acute upper respiratory tract infections is available. (aafp.org)
- Upper respiratory tract infections account for millions of visits to family physicians each year in the United States. (aafp.org)
- Upper respiratory tract infections (URIs) are commonly treated in family physicians' practices. (aafp.org)
- Protection against avian metapneumovirus subtype C in turkeys immunized via the respiratory tract with inactivated virus. (southernbiotech.com)
- The bacterium can asymptomatically colonize the upper respiratory tract and skin of humans and take advantage of opportune conditions, like immunodeficiency or breached barriers, to cause infection. (uni-wuerzburg.de)
- Upper respiratory tract infection is a nonspecific term used to describe an acute infection involving the nose, paranasal sinuses, pharynx and larynx. (scielo.br)
- Upper respiratory tract infections in children are often associated with Eustachian tube dysfunction and complicated by otitis media, an inflammatory process within the middle ear. (scielo.br)
- Environmental, epidemiologic and familial risk factors for otitis media (such as sex, socioeconomic and educational factors, smoke exposure, allergy or duration of breastfeeding) have been previously reported, but actually no data about their diffusion among Sicilian children with upper respiratory tract infections are available. (scielo.br)
- To investigate the main risk factors for otitis media and their prevalence in Sicilian children with and without upper respiratory tract infections. (scielo.br)
- A case-control study of 204 children with upper respiratory tract infections who developed otitis media during a 3 weeks monitoring period and 204 age and sex-matched healthy controls. (scielo.br)
Rate-241
- His vitals on admission: Temperature-103.8 °F, BP-138/84 (No orthostatic changes), Pulse rate- 114 and regular, Respiratory rate-24, Pulse oximetry showed oxygen saturation of 88% at room air. (ispub.com)
Gastrointestinal3
- Bacterial infections of respiratory and gastrointestinal mucosae : based on a symposium of the SGM held in September 1987 / edited by W. Donachie, E. Griffiths, J. Stephen. (who.int)
- Ingestion can cause irritation to the gastrointestinal mucosa and can be complicated by pulmonary aspiration, resulting in chemical pneumonitis. (cdc.gov)
- The National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health, invites Exploratory/Developmental Research Project (R21) applications from institutions/organizations that propose to study immune defense mechanisms and immune regulation at mucosal surfaces including the respiratory, gastrointestinal, and urogenital tracts. (nih.gov)
Mucosal2
- Jaspers' lab previously demonstrated that cigarette smoking significantly impaired the immune responses of mucosal cells within the respiratory system. (eurekalert.org)
- E-cigarette users showed the same changes in those genes, and they also demonstrated suppression of several additional immune genes, suggesting an even broader effect on the respiratory mucosal immune response system. (eurekalert.org)
Distress2
- Inhalation typically leads to respiratory distress, fever, and cough followed by the development of pulmonary edema, hypotension, respiratory failure, and possibly death within 36 to 72 hours. (cdc.gov)
- PHYSICAL EXAM: On examination, the patient was conscious, toxic and in respiratory distress. (ispub.com)
Infection3
- Unlike the respiratory viruses that cause measles, mumps and rubella-for which vaccination or recovery from illness provides decades-long protection against future infection-flu, RSV, SARS-CoV-2 and "common cold" coronaviruses share several characteristics that enable them to cause repeated re-infections. (nih.gov)
- Important sites of infection are the respiratory mucosa (respiratory diphtheria) and the skin (cutaneous diphtheria). (tn.gov)
- Using orthogonal RNA and protein expression assessments, we confirmed SARS-CoV-2 infection in the glands and mucosae. (nature.com)
Vaccines2
- Vaccines that provide long-lasting protection against influenza, coronaviruses and respiratory syncytial virus (RSV) have proved exceptionally difficult to develop. (nih.gov)
- A next generation of improved vaccines for mucosa-replicating viruses will require advances in understanding on several fronts, the authors say. (nih.gov)
Epithelium1
- Histologic evaluation of TAM sections revealed a pseudostratified respiratory epithelium consisting of ciliated, mucus-producing and basal cells. (ersjournals.com)
Upper respiratory3
- For instance, more must be learned about interactions between flu viruses, coronaviruses and RSV and the components of the immune response that operate largely or exclusively in the upper respiratory system. (nih.gov)
- Workers reported skin , eye and nose, and upper respiratory irritation. (cdc.gov)
- This article outlines the guidelines and indications for appropriate antibiotic use for common upper respiratory infections. (aafp.org)
Droplets1
- The disease is transmitted from person to person by respiratory droplets or direct contact with respiratory secretions, discharges from skin lesions or, rarely, fomites. (tn.gov)
Infections1
- Our aim was to generate a TAM that closely resembles natural airway mucosa and to establish optimal conditions for infections studies with B. pertussis. (ersjournals.com)
Larynx1
- The hallmark of respiratory diphtheria is the presence of a tough, grayish-white pseudomembrane over the tonsils, the pharynx, or larynx. (tn.gov)
Viral1
- They conclude, "we are excited and invigorated that many investigators…are rethinking, from the ground up, all of our past assumptions and approaches to preventing important respiratory viral diseases and working to find bold new paths forward. (nih.gov)
Exposure1
- Using translational human in vitro and in vivo approaches, Jaspers' lab hopes to ascertain whether long-term exposure to e-cigarettes - especially those with cinnamon-flavored e-liquids - has immune suppressive effects on the respiratory mucosa of people. (eurekalert.org)
Syndrome1
- SARS-CoV-2, severe acute respiratory syndrome coronavirus 2. (cdc.gov)
Represents1
- With respect to morphology and barrier characteristics, TAM highly represents natural human airway mucosa. (ersjournals.com)
Illness1
- Aerial transmission is another important route by which enterovirus D68 and other serotypes cause respiratory illness. (medscape.com)
Regulation1
- 3. Regulation of mucin expression in respiratory diseases. (nih.gov)
Immune2
- The chemicals compromise the immune function of key respiratory immune cells, such as macrophages, natural killer cells, and neutrophils. (eurekalert.org)
- The compromised immune function of the respiratory immune cells could signal the first in a cascade of cellular mechanisms that lead to impaired immune responses in the lung. (eurekalert.org)
Human1
- Tissue-engineered human airway models (TAM) are promising tools to investigate interrelations between B. pertussis and the airway mucosa. (ersjournals.com)
Failure1
- Withdraw the respiratory failure. (reso-nation.org)
Body2
- Message Body (Your Name) thought you would like to see the European Respiratory Society web site. (ersjournals.com)
- it affects many parts of the body, such as the whole respiratory mucosa, the kidneys, fat cells, parts of the brain. (everydayhealth.com)
Oral2
- Examination of the oral cavity revealed thrush on the buccal mucosa. (ispub.com)
- Lesions of the oral mucosa of herpetic etiology (as part of complex therapy). (abchealthonline.com)
Time1
- Time of norpace en españa. (reso-nation.org)
Surface1
- Injury can lead to a permanent reduction in gas exchange surface area and respiratory function. (nih.gov)