Regular exercise, appropriate rest, and healthy nutrition  Avoiding people currently infected with e.
This is an open access article distributed under the Creative Commons Attribution Licensewhich permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract The dioxins and dioxin-like compounds in cigarette smoke and environmental pollutants modulate immunological responses.
These environmental toxicants are known to cause lung cancer but have also recently been implicated in allergic and inflammatory diseases such as bronchitis, asthma, and chronic obstructive pulmonary disease COPD.
We have previously reported that human bronchial epithelial cells express AhR, and AhR activation induces mucin production through reactive oxygen species. This review discusses the role of AhR in asthma and COPD, focusing in particular on inflammatory and resident cells in the lung.
We describe the important impact that AhR activation may have on the inflammation phase in the pathology of asthma and COPD.
In addition, crosstalk of AhR signaling with other ligand-activated transcription factors such as peroxisome proliferator-activated receptors PPARs has been well documented.
Introduction Both allergic asthma and COPD are defined as airway inflammatory diseases; however, the inflammatory mechanism is different for each disease. Nocuous agents such as PCBs, B[a]P, and dioxin-like compounds in cigarette smoke and environmental pollutants have the potential to induce inflammation or exacerbate chronic bronchitis, asthma, COPD, and lung cancer [ 1 — 4 ].
In addition to airway epithelial cells, many inflammatory cells, including Th2 cells, eosinophils, and basophils, play a major pathophysiological role in asthma and COPD [ 5 — 8 ]. Cigarette smoke and environmental pollutants activate these inflammatory cells, and they contribute to the activation of growth factors and cytokines.
While the molecular signaling mechanism for this transcriptional modulation of cytokines remains to be determined, it has been recently recognized that these effects are mainly mediated through the binding of noxious agents to the AhR. All major human cell types express AhR, including pulmonary tissue [ 1314 ].
The liver, adipose tissue, and skin are the major storage sites of AhR ligands in humans [ 15 ]. These AhR ligands are also concentrated in bronchial epithelial cells, suggesting that the respiratory system is sensitive to AhR ligands [ 16 ].
The AhR is a ligand-activated transcription factor, and after ligation of dioxins to the AhR, the receptor translocates from the cytosol to the nucleus, where it heterodimerizes with the ARNT. CYPs convert B[a]P and dioxin-like compounds into physiologic metabolites that exert effects on cell growth, differentiation, and migration.
In this review article, we summarize current findings regarding the functional role of AhR molecules in airway inflammation and focus on bronchial epithelial cells, fibroblasts, granulocytes, and lymphocytes.
Understanding the effects of AhR on these cells would be a breakthrough in our understanding of the pathology and treatment of asthma and COPD. Airway Epithelial Cells Airway epithelial cells are able to modify allergic airway inflammation by virtue of their ability to produce a variety of inflammatory mediators [ 1819 ].
One such mediator is the moderate bronchial mucin-containing mucus, which normally protects the airway from exogenous substances.
Hypermucosis in the airway, however, is associated with several respiratory diseases, including asthma and COPD.
Mucus hypersecretion in the airway increases coughing and expectoration of sputum. Clara cells in the airway can secrete a wide variety of glycoproteins, such as mucins and SP-D, and are very sensitive to AhR stimulation [ 2021 ].
Mucus production is typically mediated by cytokine or lipid mediator release, or an increase of ROS [ 22 — 24 ].What is the relationship between vitamin D and childhood UTIs?
A new study suggests vitamin D may protect against UTIs among children by upregulating their own naturally occurring antimicrobial peptides. Omega-3 fatty acids, docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), are found naturally in fish oil and are commonly thought to be anti-inflammatory nutrients, with protective effects in inflammatory diseases including asthma and allergies.
Asthma is a common long-term inflammatory disease of the airways of the lungs. It is characterized by variable and recurring symptoms, reversible airflow obstruction, and bronchospasm.
Symptoms include episodes of wheezing, coughing, chest tightness, and shortness of breath.
These episodes may occur a few times a day or a few times per week. Depending on the person, they may become worse at. The International Journal of Chronic Obstructive Pulmonary Disease Indexed: American Chemical Society's Chemical Abstracts Service (CAS)- PubMed (files to appear soon)ISSN (Print)ISSN (Online)An international, peer-reviewed journal of therapeutics and pharmacology focusing on concise rapid reporting of .
The original evidence of a potential adverse effect of ß blockers in asthma and COPD was based on case reports of acute bronchospasm precipitated by high doses of noncardioselective ß blockers.
For this systematic review and one-step and two-step meta-analysis of individual participant data, we searched MEDLINE, Embase, the Cochrane Central Register of Controlled Trials, and Web of Science for double-blind, placebo-controlled, randomised controlled trials of vitamin D 3 or vitamin D 2 supplementation in people with asthma that reported incidence of asthma exacerbation, published.