Airway Disorders Research Articles

Sleep-disordered breathing and dental sleep medicine: Implications for oral health and overall well-being

Sleep-disordered breathing (SDB) is a prevalent condition that encompasses a range of disorders, such as snoring, obstructive sleep apnea (OSA), and upper airway resistance syndrome. These disorders have significant implications for both oral health and overall well-being. Dental sleep medicine (DSM) plays a crucial role in the identification, diagnosis, and management of SDB, offering effective treatment options for patients. As awareness grows regarding the detrimental effects of airway disorders, particularly obstructive sleep apnea (OSA), as a sleep-related breathing disorder, it becomes important to recognize the potential role of dentists in offering solutions in this field. This recognition gives rise to a new aspect of dentistry known as Dental Sleep Medicine (DSM). DSM focuses on the practice of clinical dentistry with the goal of achieving an ideal jaw relationship and establishing normal oral function and performance. One crucial aspect of function and performance is the airway and breathing, which is among the most vital functions for human beings. Any alterations in the airway and breathing patterns can lead to changes in the posture of the tongue, jaws, and head, ultimately resulting in malocclusion. Early dental treatment not only has a positive impact on the teeth but also helps establish the best possible airway at an early age. Dentists now play a crucial and integral role as part of an interdisciplinary group involved in managing Sleep-Related Breathing Disorders (SRBDs). This review article aims to provide guidance to dentists in identifying children or adults who are suspected or at risk of SRBDs. Additionally, it will explain the roles of dentists and orthodontists in the management and treatment of SRBDs.

Natural killer cells in the lung: potential role in asthma and virus-induced exacerbation?

Asthma is a chronic inflammatory airway disorder whose pathophysiological and immunological mechanisms are not completely understood. Asthma exacerbations are mostly driven by respiratory viral infections and characterised by worsening of symptoms. Despite current therapies, asthma exacerbations can still be life-threatening. Natural killer (NK) cells are innate lymphoid cells well known for their antiviral activity and are present in the lung as circulating and resident cells. However, their functions in asthma and its exacerbations are still unclear. In this review, we will address NK cell activation and functions, which are particularly relevant for asthma and virus-induced asthma exacerbations. Then, the role of NK cells in the lungs at homeostasis in healthy individuals will be described, as well as their functions during pulmonary viral infections, with an emphasis on those associated with asthma exacerbations. Finally, we will discuss the involvement of NK cells in asthma and virus-induced exacerbations and examine the effect of asthma treatments on NK cells.

Endoplasmic reticulum stress mediates environmental particle-induced inflammatory response in bronchial epithelium

While the detailed mechanisms for how particulate matter (PM) causes adverse health effects in the lungs remain largely unknown, endoplasmic reticulum (ER) stress has been implicated in PM-induced lung injury. The present study was undertaken to examine how/if ER stress might regulate PM-induced inflammation, and to begin to define potential underlying molecular mechanisms. Here, ER stress hallmarks were examined in human bronchial epithelial (HBE) cells exposed to PM. To confirm roles of certain pathways, siRNA targeting ER stress genes and an ER stress inhibitor were employed. Expression of select inflammatory cytokines and related signaling pathway components by the cells were assessed as well. The results showed that PM exposure induced elevations in two ER stress hallmarks, i.e. GRP78 and IRE1α, in time-and/or dose-related manners in the HBE cells. Inhibition of ER stress by siRNA for GRP78 or IRE1α significantly alleviated the PM-induced effects. Further, ER stress appeared to regulate PM-induced inflammation – likely through downstream autophagy and NF-κB pathways – as implied by studies showing that inhibition of ER stress by siRNA of GRP78 or IRE1α caused significant amelioration of PM-induced autophagy and subsequent activation of NF-κB pathways. Moreover, the ER stress inhibitor 4-PBA were used to confirm the protective effects against PM-induced outcomes. Together, the results suggest ER stress plays a deleterious role in PM-induced airway inflammation, possibly through activation of autophagy and NF-κB signaling. Accordingly, protocols/treatments that could lead to inhibited ER stress could potentially be effective for treatment of PM-related airway disorders.

Ambroxol therapy for Parkinson’s disease: Systematic literature review

Parkinson’s disease (PD) is the second most common neurodegenerative disease. The accumulation of α-synuclein protein in the basal ganglia is the underlying pathogenesis of PD. Genetic abnormalities are one of the predisposing factors for PD. PDs with GBA gene mutations have abnormalities coding for β-glucocerebrosidase (GCase) enzymes in lysosomes, which lead to increased accumulation of α-synuclein. Ambroxol has long been known as a therapy for airway disorders which also has antioxidant benefits. However, recently, there have been many experimental studies examining the benefits of ambroxol in neurodegenerative diseases, including PD. This study aims to examine experimental studies of ambroxol administration in PD.

Accuracy of Triage in Service in The Emergency Department (Literature Review)

Service accuracy is the minimum standard of service that must be achieved by nurses in the emergency room, so that proper triage implementation is needed. Triage is the classification of patients based on the level of emergency by prioritising actions on airway (A), breathing (B), and circulation (C) disorders by considering facilities, human resources and the probability of patient life. The literature search in this literature review uses six databases with high and medium quality criteria, namely scient driect, IEEG, cedekia, Sci-hub, ProQuest, Pubmed. For previous studies using correlational analytics with a cross-sectional study approach, descriptive: combination (mixed methods) with sequential explanatory design. cross sectional. Check Prisma to guide this review. Titles, abstracts, full text and methodology were assessed for study eligibility. Data were tabulated and analysed narratively. Results: Nine journal literature met the inclusion criteria, with the major theme of triage accuracy in the Emergency Department. There were three journals analysing the accuracy of triage implementation, and four journals relating to triage accuracy. Factors that often appear in triage accuracy include nurses' understanding of triage, motivation and workload. Knowledge is one of the most important factors in the accuracy of triage implementation. Proper implementation of triage can reduce morbidity, disability, and mortality so as to improve service quality and customer satisfaction.
 
 Keywords: Accuracy of triage.

Myeloid-Specific SIRT6 Deletion Protects Against Particulate Matter (PM2.5)-Induced Airway Inflammation.

Particulate matter (PM2.5) is a common risk factor for airway inflammation. Alveolar macrophages play a critical role in airway inflammation. Sirtuin 6 (SIRT6) is a class Ill histone deacetylase that exerts an anti-inflammatory effect in airway diseases. However, the role of SIRT6 on PM2.5-induced airway inflammation in macrophages remains unclear. We aimed to determine whether SIRT6 protects against PM2.5-induced airway inflammation in macrophages. The effect of SIRT6 on PM2.5-induced airway inflammation was assessed by using THP1 cells or bone marrow-derived macrophages (BMDMs) exposed to PM2.5 in vitro and myeloid cell-specific SIRT6 conditional knockout mice (Sirt6fl/fl-LysMCre) in vivo. PM2.5 increased SIRT6 expression in THP1 cells, but SIRT6 gene silencing decreased PM2.5 induced inflammatory cytokines in THP1 cells. Moreover, the expression of SIRT6 and inflammatory cytokines was also decreased in BMDMs with myeloid-specific deletion of SIRT6 after stimulation of PM2.5. In vivo, Sirt6fl/fl-LysMCre mice substantially decreased airway inflammation in response to PM2.5 exposure. Our results revealed that SIRT6 promotes the PM2.5-induced airway inflammation in macrophages and indicated that inhibition of SIRT6 in macrophages may represent therapeutic strategy for airway disorders induced by airborne particulate pollution.

Cardiorespiratory dysautonomia in post-COVID-19 condition: Manifestations, mechanisms and management.

A significant proportion of COVID-19 patients experience debilitating symptoms for months after the acute infection. According to recent estimates, approximately one out of ten COVID-19 convalescents reports persistent health issues more than three months after initial recovery. This "post-COVID-19 condition" may include a large variety of symptoms from almost all domains and organs, and for some patients it may mean prolonged sick-leave, homestay, and strongly limited activities of daily life. In this narrative review, we focus on the symptoms and signs of post-COVID-19 condition in adults-particularly those associated with cardiovascular and respiratory systems, such as postural orthostatic tachycardia syndrome (POTS) or airway disorders-and explore the evidence for chronic autonomic dysfunction as a potential underlying mechanism. The most plausible hypotheses regarding cellular and molecular mechanisms behind the wide spectrum of observed symptoms-such as lingering viruses, persistent inflammation, impairment in oxygen sensing systems and circulating antibodies directed to blood pressure regulatory components-are discussed. In addition, an overview of currently available pharmacological and non-pharmacological treatment options is presented. This article is protected by copyright. All rights reserved.

Evaluation of airway involvement and treatment in patients with relapsing polychondritis

Airway involvement in relapsing polychondritis (RP) can be debilitating and life threatening, often requiring interventional procedures. If standard therapies including systemic corticosteroid and immunosuppressive agents are ineffective, airway stenting is often required. Recently, biologics have been reported to be effective for RP, and the early administration of biologics may avoid airway stenting. To evaluate survival rates and treatment approaches, medical records of RP patients with airway involvement were reviewed. These cases were divided into the following groups: with and without malacia, stenting and non-stenting, and with and without biologics. Kaplan–Meier was used to calculate survival rates and log rank tests were used to analyze biologics groups. A total of 77 patients were enrolled. Airway stenting was performed in 13 patients, all of which developed airway malacia. The stenting group had significantly lower survival rates than the non-stenting group (p < 0.001). Stent-related complications were granulation tissue (85%) and mucostasis (69%). In the non-stenting group, a lower mortality rate was observed. A significantly higher survival rate was seen in patients administered biologics than without (p = 0.014). The early administration of biologics shows promise in preventing severe airway disorders that require airway stenting.

Analysis of influencing factors and a predictive model of small airway dysfunction in adults

BackgroundSmall airway dysfunction (SAD) is a widespread but less typical clinical manifestation of respiratory dysfunction. In lung diseases, SAD can have a higher-than-expected impact on lung function. The aim of this study was to explore risk factors for SAD and to establish a predictive model.MethodsWe included 1233 patients in the pulmonary function room of TangDu Hospital from June 2021 to December 2021. We divided the subjects into a small airway disorder group and a non-small airway disorder group, and all participants completed a questionnaire. We performed univariate and multivariate analyses to identify the risk factors for SAD. Multivariate logistic regression was performed to construct the nomogram. The performance of the nomogram was assessed and validated by the Area under roc curve (AUC), calibration curves, and Decision curve analysis (DCA).ResultsOne. The risk factors for small airway disorder were advanced age (OR = 7.772,95% CI 2.284–26.443), female sex (OR = 1.545,95% CI 1.103–2.164), family history of respiratory disease (OR = 1.508,95% CI 1.069–2.126), history of occupational dust exposure (OR = 1.723,95% CI 1.177–2.521), history of smoking (OR = 1.732,95% CI 1.231–2.436), history of pet exposure (OR = 1.499,95% CI 1.065–2.110), exposure to O3 (OR = 1.008,95% CI 1.003–1.013), chronic bronchitis (OR = 1.947,95% CI 1.376–2.753), emphysema (OR = 2.190,95% CI 1.355–3.539) and asthma (OR = 7.287,95% CI 3.546–14.973). 2. The AUCs of the nomogram were 0.691 in the training set and 0.716 in the validation set. Both nomograms demonstrated favourable clinical consistency. 3.There was a dose‒response relationship between cigarette smoking and SAD; however, quitting smoking did not reduce the risk of SAD.ConclusionSmall airway disorders are associated with age, sex, family history of respiratory disease, occupational dust exposure, smoking history, history of pet exposure, exposure to O3, chronic bronchitis, emphysema, and asthma. The nomogram based on the above results can effectively used in the preliminary risk prediction.

The clinical efficacy of type 2 monoclonal antibodies in eosinophil-associated chronic airway diseases: a meta-analysis.

Anti-type 2 inflammation therapy has been proposed as a treatment strategy for eosinophil-associated chronic airway disorders that could reduce exacerbations and improve lung function. We performed a meta-analysis of randomized controlled trials to assess the effectiveness of type 2 monoclonal antibodies (anti-T2s) for eosinophil-associated chronic airway disorders. PubMed, Embase, Web of Science, and Cochrane Library were searched from their inception to 21 August 2022. Randomized clinical trials evaluating the effectiveness of anti-T2s versus placebo in the treatment of chronic airway diseases were selected. The outcomes were exacerbation rate and change in pre-bronchodilator forced expiratory volume in 1 s (FEV1) from baseline. The Cochrane Risk of Bias Assessment Tool 1.0 was used to evaluate the risk of bias, and the random-effects or fixed-effect model were used to pool the data. Thirty-eight articles concerning forty-one randomized clinical trials with 17,115 patients were included. Compared with placebo, anti-T2s therapy yielded a significant reduction in exacerbation rate in COPD and asthma (Rate Ratio (RR)=0.89, 95%CI, 0.83-0.95, I2 = 29.4%; RR= 0.59, 95%CI, 0.52-0.68, I2 = 83.9%, respectively) and improvement in FEV1 in asthma (Standard Mean Difference (SMD)=0.09, 95%CI, 0.08-0.11, I2 = 42.6%). Anti-T2s therapy had no effect on FEV1 improvement in COPD (SMD=0.05, 95%CI, -0.01-0.10, I2 = 69.8%). Despite inconsistent findings across trials, anti-T2s had a positive overall impact on patients' exacerbation rate in asthma and COPD and FEV1 in asthma. Anti-T2s may be effective in treating chronic airway illnesses related to eosinophils. https://www.crd.york.ac.uk/PROSPERO/, identifier CRD42022362280.

Interoception, Voice Symptom Reporting, and Voice Disorders

Interoception may play a role in how individuals perceive their voice disorder. The first objective of this study was to investigate relationships between interoception and voice disorder class (functional, structural, neurological). The second objective was to determine relationships between interoception and voice-related outcome measures between patients with functional voice and upper airway disorders and typical voice users. The third objective was to determine whether patients with primary muscle tension dysphonia (a type of functional voice disorder) had different levels of interoceptive awareness than typical voice users. Prospective cohort study. One hundred subjects with voice disorders completed the multidimensional assessment of interoceptive awareness-2 (MAIA-2). Voice diagnosis and singing experience were also acquired from each patient's medical chart. Voice handicap (VHI-10) and Part 1 of the vocal fatigue index (VFI-Part1) scores were obtained from patients diagnosed with functional voice and upper airway disorders. MAIA-2, VHI-10, VFI-Part1, and singing experience were also obtained from 25 typical voice users. Multivariable linear regression models were used to assess the association between response variables and voice disorder class, adjusting for singing experience, gender, and age. There were no significant group differences between voice disorder class (functional, structural, neurological) after adjusting for multiple comparisons. Participants with functional voice and upper airway disorders who scored significantly higher on the VHI-10 and VFI-Part1 had lower Attention Regulation sub-scores on the MAIA-2 (P's<0.05). Patients with primary muscle tension dysphonia scored significantly lower on the Emotional Awareness MAIA-2 subscale than typical voice users (P=0.005). Patients with functional voice disorders with lower capabilities to attend to body sensations may score higher on voice-related patient-reported outcome measures, like the VHI-10 and VFI-Part1. Patients with primary muscle tension dysphonia may also have lower capabilities in processing their body sensations than typical voice users.

Sputum Interleukin-32 in childhood asthma: correlation with IL-1β

_Background:_ Asthma is an airway disorder where inflammatory cytokines are partly responsible for exacerbating the disease. Interleukin (IL)-32, generally referred to as natural killer cell (NK4) transcript 4, is described as an immunoregulator involved in the stimulation of anti-/pro-inflammatory cytokines. The abnormal presence of IL-32 has been observed during inflammatory diseases, particularly in asthma. This study aims to characterize IL-32 in the inflammatory process in patients with severe asthma. _Methods:_ IL-32 and IL-1β levels in the supernatant of induced sputum obtained from 59 asthma patients (mild: 20 patients; moderate: 20 patients; severe: 19 patients) were measured using ELISA. Sputum IL-32 mRNA expression was measured by RT- PCR. _Results:_ Sputum IL-32 was significantly elevated at the protein (_p= 0.00019_) and mRNA expression (_p &lt; 0.0001_) in asthmatics compared to non-asthmatic controls. IL-32 was elevated in severe asthmatic patients (_p &lt; 0.0001_) compared to mild-moderate asthma. Severe asthmatics allergic to house dust mites expressed higher sputum IL-32 levels than severe asthmatics without allergy (_p = 0.0001_). A significant association was found between sputum IL-32 and IL-32 mRNA (r =0.531_; p = 0.0159_) in severe asthma. In the same way, sputum IL-1β and IL-32 were significantly correlated (r = 0.476; _p = 0.0337_). _Conclusion:_ The level of IL-32 in induced sputum may be associated with asthma severity.

Sputum Interleukin-32 in childhood asthma: correlation with IL-1β

_Background:_ Asthma is an airway disorder where inflammatory cytokines are partly responsible for exacerbating the disease. Interleukin (IL)-32, generally referred to as natural killer cell (NK4) transcript 4, is described as an immunoregulator involved in the stimulation of anti-/pro-inflammatory cytokines. The abnormal presence of IL-32 has been observed during inflammatory diseases, particularly in asthma. This study aims to characterize IL-32 in the inflammatory process in patients with severe asthma. _Methods:_ IL-32 and IL-1β levels in the supernatant of induced sputum obtained from 59 asthma patients (mild: 20 patients; moderate: 20 patients; severe: 19 patients) were measured using ELISA. Sputum IL-32 mRNA expression was measured by RT- PCR. _Results:_ Sputum IL-32 was significantly elevated at the protein (_p= 0.00019_) and mRNA expression (_p &lt; 0.0001_) in asthmatics compared to non-asthmatic controls. IL-32 was elevated in severe asthmatic patients (_p &lt; 0.0001_) compared to mild-moderate asthma. Severe asthmatics allergic to house dust mites expressed higher sputum IL-32 level than severe asthmatics without allergy (_p = 0.0001_). A significant association was found between sputum IL-32 and IL-32 mRNA (r =0.531_; p = 0.0159_) in severe asthma. In the same way, sputum IL-1β and IL-32 were significantly correlated (r = 0.476; _p = 0.0337_). _Conclusion:_ The level of IL-32 in induced sputum may be associated with asthma severity.

Exploring the immunological basis of periodic fever, aphthous stomatitis, pharyngitis, and adenitis (PFAPA) syndrome: immunohistochemical staining features of palatine tonsils.

Periodic fever, aphthous stomatitis, pharyngitis, and adenitis (PFAPA) syndrome is the most common periodic fever syndrome during early childhood period with regular febrile attacks of sterile upper airway inflammation. The cessation of attacks following tonsillectomy points to fundamental role of tonsil tissue on etiopathogenesis of disease, which is not clarified satisfactorily. The aim of this study is to explore the immunological basis of PFAPA by evaluating the cellular properties of tonsils, and microbial exposition such as Helicobacter pylori on tonsillectomy materials. The paraffinized tonsil samples of 26 PFAPA and 29 control patients with obstructive upper airway disorder were compared in terms of immunohistochemical staining features including CD4, CD8, CD123, CD1a, CD20, and H. pylori. The median number of CD8+ cells was 1485 (1218-1287) in PFAPA while it was 1003 (852-1261.5) in control group and the difference was statistically significant (p=0.001). Similarly, CD4+ cell counts were statistically higher in PFAPA group than control (833.5 vs 622). The ratio of CD4/CD8 did not differ between two groups; also, there was no statistically difference in terms of the other immunohistochemical staining results, such as CD20, CD1a, CD123 and H. pylori. This is the largest number of pediatric tonsillar tissue study of PFAPA patients in current literature and we emphasized the triggering effects of CD8+ and CD4+ T-cells on PFAPA tonsils. • The cessation of attacks following tonsillectomy points to fundamental role of tonsil tissue on etiopathogenesis of disease, which is not clarified satisfactorily. • In current study, 92.3% of our patients did not experience any attacks following operation similarly with literature. • We observed the increased number of CD4+ and CD8+ T cell counts on PFAPA tonsils compared to control group and emphasized the active role of both CD4+ and CD8+ cells localized on PFAPA tonsils in immune dysregulation. • Some other cell types evaluated in this study such as CD19+ (B cells), CD1a (dendritic cells), and CD123 (IL-3 receptors, for pluripotent stem cells) and H. pylori did not differ in PFAPA patients compared to the control group.

Sputum Interleukin-32 in childhood asthma: correlation with IL-1β

_Background:_ Asthma is an airway disorder where inflammatory cytokines are partly responsible for exacerbating the disease. Interleukin (IL)-32, generally referred to as natural killer cell (NK4) transcript 4, is described as an immunoregulator involved in the stimulation of anti-/pro-inflammatory cytokines. The abnormal presence of IL-32 has been observed during inflammatory diseases, particularly in asthma. This study aims to characterize IL-32 in the inflammatory process in patients with severe asthma. _Methods:_ IL-32 and IL-1β levels in the supernatant of induced sputum obtained from 59 asthma patients (mild: 20 patients; moderate: 20 patients; severe: 19 patients) were measured using ELISA. Sputum IL-32 mRNA expression was measured by RT- PCR. _Results:_ Sputum IL-32 was significantly elevated at the protein (_p= 0.00019_) and mRNA expression (_p &lt; 0.0001_) in asthmatics compared to non-asthmatic controls. IL-32 was elevated in severe asthmatic patients (_p &lt; 0.0001_) compared to mild-moderate asthma. Severe asthmatics allergic to house dust mites expressed higher sputum IL-32 level than severe asthmatics without allergy (_p = 0.0001_). A significant association was found between sputum IL-32 and IL-32 mRNA (r =0.531_; p = 0.0159_) in severe asthma. In the same way, sputum IL-1β and IL-32 were significantly correlated (r = 0.476; _p = 0.0337_). _Conclusion:_ The level of IL-32 in induced sputum may be associated with asthma severity.

MiR-214 Expression Is Elevated in Chronic Rhinosinusitis Mucosa and Regulates Lipopolysaccharide-Mediated Responses in Undifferentiated Human Nasal Epithelial Cell Culture.

Chronic rhinosinusitis (CRS) is an inflammatory disorder of the upper airways. MicroRNAs (miRs) are reported to regulate several diverse physiological and pathological processes. This study aimed to evaluate the impact of miR-214 on lipopolysaccharide (LPS)-mediated inflammation, and mucin 5AC (MUC5AC) expression in human nasal epithelial cells. The expression of miR-214 was detected in CRS with polyps (CRSwNP) and CRS without polyps (CRSsNP) tissues. Cells were treated with LPS and a miR-214 inhibitor. The level of miR-214 was detected by quantitative real-time reverse transcriptase-PCR (qRT-PCR). The inflammatory cytokines (IL-6, IL-8, TNF, and IL-1β) and MUC5AC production were determined by qRT-PCR and ELISA. MUC5AC protein level was detected using western blot. Similarly, we determined the relationship between miR-214 and Sirtuin 1 (SIRT1) using the Dual luciferase activity assay. miR-214 was increased in CRSwNP and CRSsNP tissues. LPS triggered the expression of miR-214, while miR-214 inhibition diminished the level of miR-214. MiR-214 inhibition prevented LPS-mediated the production of inflammatory cytokines. LPS treatment augmented MUC5AC mRNA, protein levels, and secretion, whereas miR-214 loss inhibited MUC5AC production in the presence of LPS. SIRT1 is a direct target of miR-214. Impairing SIRT1 by siRNA (siSIRT1) or EX527 (a selective SIRT1 inhibitor) reversed the effects of miR-214 inhibitor on inflammation and MUC5AC expression. Furthermore, miR-214 depression inhibited the STAT3/GDF15 pathway via targeting SIRT1. Upregulation of STAT3 or GDF15 partly abolished the anti-inflammatory roles of miR-214 inhibitor. Taken together, miR-214 regulates LPS-mediated inflammation and MUC5AC expression via targeting SIRT1, and STAT3/GDF15 may involve in the regulation of miR-214 inhibitor on inflammation and MUC5AC expression.

CXCL12/CXCR4 Axis is Involved in the Recruitment of NK Cells by HMGB1 Contributing to Persistent Airway Inflammation and AHR During the Late Stage of RSV Infection.

We previously showed that both high-mobility group box-1 (HMGB1) and natural killer (NK) cells contribute to respiratory syncytial virus (RSV)-induced persistent airway inflammation and airway hyperresponsiveness (AHR). Meanwhile, Chemokine (C-X-C motif) ligand 12 (CXCL12) and its specific receptor (chemokine receptor 4, CXCR4) play important roles in recruitment of immune cells. CXCL12 has been reported to form a complex with HMGB1 that binds to CXCR4 and increases inflammatory cell migration. The relationship between HMGB1, NK cells and chemokines in RSV-infected model remains unclear. An anti-HMGB1 neutralizing antibody and inhibitor of CXCR4 (AMD3100) was administered to observe changes of NK cells and airway disorders in nude mice and BALB/c mice. Results showed that the mRNA expression and protein levels of HMGB1 were elevated in late stage of RSV infection and persistent airway inflammation and AHR were diminished after administration of anti-HMGB1 antibodies, with an associated significant decrease in CXCR4+ NK cells. In addition, CXCL12 and CXCR4 were reduced after HMGB1 blockade. Treatment with AMD3100 significantly suppressed the recruitment of NK cells and alleviated the airway disorders. Thus, CXCL12/CXCR4 axis is involved in the recruitment of NK cells by HMGB1, contributing to persistent airway inflammation and AHR during the late stage of RSV infection.

Determination of MDA as oxidative stress marker and most common type of blood group in asthmatic patients before and after treatment with montelukast drug.

Asthma is a complex chronic inflammatory disorder of airways characterized by airway smooth muscle hypertrophy, hyperplasia and over production of mucous in which many cells and cellular elements play an important role.&#x0D; The aim of the study is to monitor the changes in asthmatic patients before and after treatment with montelukast in the MDA level as oxidative stress marker in asthmatic cases, and the most common type of blood group. The total number of subjects included in this study was two hundred with acute asthma. The major part of this study represents a follow up study.&#x0D; Subjects with bronchial asthma were previously diagnosed but not on regular treatment, their aged ranged between (16 – 50) years attending the respiratory unit directly at tikrit teaching hospital. The period of data collection was from first of April of 2013 up to the mid of June- 2014.&#x0D; There is a significant change in level of MDA, during the asthmatic attacks (1.12± 0.42, while after treatment (0.6 ± 0.34 P ≤ 0.001). The most common type of blood group in asthmatic cases is type O which about 69% from total number of cases , type A about 18.5%, type B about 9% , and type AB about 3.5%).

Association of ANRIL Gene Single-Nucleotide Polymorphisms With Allergic Rhinitis in Kurdish Population From Kermanshah, Iran.

Allergic rhinitis (AR) is the most common inflammatory disorder of the upper airway caused by aberrant immune responses to allergens in genetically predisposed individuals. Recently, the long noncoding RNA (lncRNA) antisense noncoding RNA in the INK4 locus (ANRIL) has been identified as a novel genetic factor associated with increased AR risk. This study aimed to evaluate the potential correlation of ANRIL gene single nucleotide polymorphisms (SNPs) with AR risk in the Kurdish population of Kermanshah, Iran. In this case-control study, 130 AR patients and 130 healthy controls were recruited to genotype for two SNPs of the ANRIL gene (rs1333048 and rs10757278) using the Tetra-primer amplification refractory mutation system polymerase chain reaction (T-ARMS-PCR) method. Our results showed no significant difference for the alleles and genotypes frequency distribution of lncRNA ANRIL SNPs (rs1333048 and rs10757278) between AR patients and healthy controls (p > 0.05). Additionally, the dominant, additive and recessive genetic models of both SNPs were not associated with altered susceptibility to AR risk (p > 0.05). The results demonstrated that the ANRIL gene rs1333048 and rs10757278 polymorphisms might not be associated with susceptibility to AR in the Kurdish population of Kermanshah, Iran.

Helicobacter pylori infection in chronic obstructive pulmonary disease

Context Chronic obstructive pulmonary disease (COPD) is a prevalent condition defined by chronic respiratory symptoms and difficult airflow caused by airway and/or alveolar disorders. Helicobacter pylori infection is a chronic stomach inflammation, which dramatically changes the gastric immune reaction, potentially leading to systemic consequences. Aims The study’s goal was to identify the effect of H. pylori infection in the severity of COPD. Settings and design Ain Shams University Hospital, a case–control observational study. Patients and methods The current study involved 40 patients who were diagnosed as COPD and 40 individuals as healthy controls with matched age and sex. All participants were evaluated by clinical assessment, chest radiograph, H. pylori stool Ag test, and spirometry with pre-bronchodilator and post-bronchodilator test. Statistical analysis used To compare quantitative variables unpaired t test was used and for qualitative variables χ 2 test was used. Results H. pylori test results in patients and controls showed that 27 (67.5%) and 24 (60.0%) individuals were seropositive without significance between them. Seropositive H. pylori between the stages of COPD were 50% in the mild stage, 70% in the moderate stage, 70% in the severe stage, and 80% in the very severe stage, with no significant difference regarding the relation between the of H. pylori infection and severity of COPD. Conclusion There is high incidence of H. pylori infection in COPD patients and may have a role in the initiation and worsening of COPD in predisposed patients without significant relation between H. pylori and severity of COPD.