The role of inhaled steroids in patients with chronic respiratory diseases is a matter of debate due to the potential effect on the development and prognosis of community-acquired pneumonia (CAP). We assessed whether treatment with inhaled steroids in patients with chronic bronchitis, COPD or asthma and CAP may affect early outcome of the acute pneumonic episode.
Respiratory disease is the leading cause of death in the UK. Methods for assessing pulmonary function and chest wall movement are essential for accurate diagnosis, as well as monitoring response to treatment, operative procedures and rehabilitation. Despite this, there is a lack of low-cost devices for rapid assessment. Spirometry is used to measure air flow expired, but cannot infer or directly measure full chest wall motion. This paper presents the development of a low-cost chest wall motion assessment system. The prototype was developed using four Microsoft Kinect sensors to create a 3D time-varying representation of a patient’s torso. An evaluation of the system in two phases is also presented. Initially, static volume of a resuscitation mannequin with that of a Nikon laser scanner is performed. This showed the system has slight underprediction of 0.441 %. Next, a dynamic analysis through the comparison of results from the prototype and a spirometer in nine cystic fibrosis patients and thirteen healthy subjects was performed. This showed an agreement with correlation coefficients above 0.8656 in all participants. The system shows promise as a method for assessing respiratory disease in a cost-effective and timely manner. Further work must now be performed to develop the prototype and provide further evaluations.
Influenza A virus (IAV) neuraminidase (NA) cleaves sialic acids (Sias) from glycans. Inhibiting NA with oseltamivir suppresses both viral infection, and viral release from cultured human airway epithelial cells. The role of NA in viral exit is well established: it releases budding virions by cleaving Sias from glycoconjugates on infected cells and progeny virions. The role of NA in viral entry remains unclear. Host respiratory epithelia secrete a mucus layer rich in heavily sialylated glycoproteins; these could inhibit viral entry by mimicking sialylated receptors on the cell surface. It has been suggested that NA allows influenza to penetrate the mucus by cleaving these sialylated decoys, but the exact mechanism is not yet established.
Preterm birth is the leading cause of neonatal mortality, and is frequently associated with intra-amniotic infection hypothesized to arise from bacterial ascension across a dysfunctional cervical mucus plug. To study this dysfunction, we assessed the permeability of cervical mucus from non-pregnant ovulating (n = 20) and high- (n = 9) and low-risk (n = 16) pregnant women to probes of varying sizes and surface chemistries. We found that the motion of negatively charged, carboxylated microspheres in mucus from pregnant patients was significantly restricted compared to ovulating patients, but not significantly different between high- and low-risk pregnant women. In contrast, charged peptide probes small enough to avoid steric interactions, but sensitive to the biochemical modifications of mucus components exhibited significantly different transport profiles through mucus from high- and low-risk patients. Thus, although both microstructural rearrangements of the components of mucus as well as biochemical modifications to their adhesiveness may alter the overall permeability of the cervical mucus plug, our findings suggest that the latter mechanism plays a dominant role in the impairment of the function of this barrier during preterm birth. We expect that these probes may be readily adapted to study the mechanisms underlying disease progression on all mucosal epithelia, including those in the mouth, lungs, and gut.
- American journal of respiratory and critical care medicine
- Published about 1 month ago
Cleaning tasks may imply exposure to chemical agents with potential harmful effects to the respiratory system, and increased risk of asthma and respiratory symptoms among professional cleaners and in persons cleaning at home has been reported. The long-term consequences of cleaning agents on respiratory health are, however, not well described.
Rebound congestion and rhinitis medicamentosa: Nasal decongestants in clinical practice. Critical review of the literature by a medical panel
- European annals of otorhinolaryngology, head and neck diseases
- Published about 5 years ago
INTRODUCTION: Systemic and topical nasal decongestants are widely used in otorhinolaryngology and general practice for the management of acute rhinosinusitis and as an adjuvant in certain forms of chronic rhinosinusitis. These products, very effective to rapidly improve nasal congestion, are sometimes available over the counter and can be the subject of misuse, which is difficult to control. The Société Française d'ORL has recently issued guidelines concerning the use of these decongestants in the doctor’s office and the operating room. MATERIALS AND METHODS: The review of the literature conducted by the task force studied in detail the concepts of “rebound congestion” and “rhinitis medicamentosa” often reported in a context of misuse, particularly of topical nasal decongestants. The clinical and histopathological consequences of prolonged and repeated use of nasal decongestants have been studied on animal models and healthy subjects. RESULTS: Discordant results have been obtained, as some authors reported a harmful effect of nasal decongestants on the nasal mucosa, while others did not identify any significant changes. No study has been able to distinguish between inflammatory lesions induced by chronic rhinosinusitis and lesions possibly related to the use of nasal decongestants. DISCUSSION: The task force explained the rebound congestion observed after stopping nasal decongestant treatment by return of the nasal congestion induced by rhinosinusitis and rejected the concept of rhinitis medicamentosa in the absence of scientific evidence from patients with rhinosinusitis. CONCLUSION: Nasal decongestants are recommended for the management of acute rhinosinusitis to reduce the consequences of often disabling nasal congestion. They are also recommended during rhinoscopic examination and for preparation of the nasal mucosa prior to endonasal surgery.
Innate immune signaling pathways contribute to the protection of host tissue when bacterially challenged. Colonic goblet cells are responsible for generating the two mucus layers that physically separate the luminal microbiota from the host epithelium. Analysis of colonic tissues from multiple mouse strains allowed us to identify a “sentinel” goblet cell (senGC) localized to the colonic crypt entrance. This cell nonspecifically endocytoses and reacts to the TLR2/1, TLR4, and TLR5 ligands by activating the Nlrp6 inflammasome downstream of TLR- and MyD88-dependent Nox/Duox reactive oxygen species synthesis. This triggers calcium ion-dependent compound exocytosis of Muc2 mucin from the senGC and generates an intercellular gap junction signal; in turn, this signal induces Muc2 secretion from adjacent goblet cells in the upper crypt, which expels bacteria. Thus, senGCs guard and protect the colonic crypt from bacterial intruders that have penetrated the inner mucus layer.
The intestinal mucosal barrier controlling the resident microbiome is dependent on a protective mucus layer generated by goblet cells, impairment of which is a hallmark of the inflammatory bowel disease, ulcerative colitis. Here, we show that IL-18 is critical in driving the pathologic breakdown of barrier integrity in a model of colitis. Deletion of Il18 or its receptor Il18r1 in intestinal epithelial cells (Δ/EC) conferred protection from colitis and mucosal damage in mice. In contrast, deletion of the IL-18 negative regulator Il18bp resulted in severe colitis associated with loss of mature goblet cells. Colitis and goblet cell loss were rescued in Il18bp(-/-);Il18r(Δ/EC) mice, demonstrating that colitis severity is controlled at the level of IL-18 signaling in intestinal epithelial cells. IL-18 inhibited goblet cell maturation by regulating the transcriptional program instructing goblet cell development. These results inform on the mechanism of goblet cell dysfunction that underlies the pathology of ulcerative colitis.
Theileriosis is an economically important hemoprotozoal disease with high morbidity and mortality in cattle. The present study reported the pathological features of a natural outbreak of tropical bovine theileriosis due to Theileria annulata in Fars Province, southern Iran. T. annulata was confirmed by the presence of T. annulata piroplasms in the blood smears and also by polymerase chain reaction test. On necropsy, pale mucous membranes and petechial and ecchymotic hemorrhages in the mucosal and serosal surfaces together with lymphadenopathy were observed. The liver was friable, yellowish, and larger than normal. Hemorrhages and punched-out ulcers were observed in the abomasal mucous membrane. Severe petechial hemorrhages were seen in the skin particularly in the hairless areas. Pulmonary edema and emphysema with petechial and ecchymotic hemorrhagic foci in the lungs were evident. The main histological changes were proliferation of lymphocytes in the lymph nodes and proliferation of macrophages, lymphocytes, and plasma cells in the spleen, Peyer’s patches, portal tracts of the liver, and interstitial tissue of the kidneys. The mucous membrane of the abomasum showed numerous multifocal areas of necrosis and ulceration, and the submucosal area and lamina propria adjacent to these lesions showed hyperemia and hemorrhages, with mononuclear cell infiltration. The skin showed multifocal necrotic changes, petechial and ecchymotic hemorrhages, and chronic dermatitis. The schizonts of Theileria were evident in the cytoplasm of the lymphocytes and macrophages of the lymph nodes, spleen, and skin. Molecular examination revealed that these animals were infected with T. annulata. The present study describes the clinicopathological findings of bovine tropical theileriosis in an unpredictable weather condition.
This report describes a case of gossypiboma in the septum. A 31-year-old woman presented with nasal obstruction and crusting that started 2 years previously after she underwent rhinoseptoplasty in another private clinic. Physical examination disclosed remaining posterior septal deviation to the left side with septal mucosal erosion on the left side. Under general anesthesia, the septal flap was elevated on the left side of the nasal cavity. A gossypiboma was found around the perpendicular ethmoid plate and between the septal flaps. The perpendicular ethmoid plate was resected and the gossypiboma was removed under endoscopy. Because of severe adhesion between the gossypiboma and the septal mucosa, removal of the gossypiboma resulted in a defect on the left mucoperichondrial flap. Right inferior turbinate mucosa was harvested and grafted on the mucosal defect of the left side. Five months after the operation, the nasal cavity showed a straight septum with a well-healed mucosa without any nasal symptoms. This case is a reminder of the fundamental importance of absolute care at every step of rhinologic surgery.