A5066081846- Asthma and respiratory diseases
- Chronic Obstructive Pulmonary Disease (COPD) Research
- Pediatric health and respiratory diseases
- Immune Response and Inflammation
- IL-33, ST2, and ILC Pathways
- Immune Cell Function and Interaction
- Allergic Rhinitis and Sensitization
- T-cell and B-cell Immunology
- Neonatal Respiratory Health Research
- Respiratory viral infections research
- Cannabis and Cannabinoid Research
- Monoclonal and Polyclonal Antibodies Research
- Immunotherapy and Immune Responses
- Gut microbiota and health
- Influenza Virus Research Studies
- Neuroscience of respiration and sleep
- Reproductive Biology and Fertility
- Respiratory Support and Mechanisms
- Inhalation and Respiratory Drug Delivery
- Respiratory and Cough-Related Research
- Eosinophilic Esophagitis
- Immune cells in cancer
- Dermatology and Skin Diseases
- Pneumonia and Respiratory Infections
- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
McMaster University
2015-2024
Hamilton Health Sciences
2024
St. Joseph’s Healthcare Hamilton
2013-2023
McMaster University Medical Centre
2013-2023
Institute for Respiratory Health
2018-2023
St Joseph's Health Care
2015-2023
First Affiliated Hospital of Guangzhou Medical University
2020-2021
State Key Laboratory of Respiratory Disease
2020-2021
Guangzhou Medical University
2020-2021
Faculty of Public Health
2011
Abstract Transforming growth factor-β1 plays a key role in the pathogenesis of pulmonary fibrosis, mediating extracellular matrix (ECM) gene expression through series intracellular signaling molecules, including Smad2 and Smad3. We show that Smad3 null mice (knockout (KO)) develop progressive age-related increases size alveolar spaces, associated with high spontaneous presence metalloproteinases (MMP-9 MMP-12) lung. Moreover, transient overexpression active TGF-β1 lungs, using adenoviral...
The purpose of this study was to explore whether repeated exposure aerosolized ovalbumin (OVA) in the context local expression GM-CSF can initiate a Th2-driven, eosinophilic inflammation airways. On day -1, Balb/c mice were infected intranasally with an adenovirus construct expressing (Ad/GM-CSF). From 0 9 exposed daily OVA aerosol. Mice alone did not show any evidence airway inflammation. receiving both Ad/GM-CSF and exhibited marked characterized by eosinophilia goblet cell hyperplasia....
Selective accumulation of eosinophils and activated CD4+ cells is now considered a central event in the pathogenesis asthma, this process thought to be mediated by number cytokines including tumor necrosis factor-alpha (TNF-alpha), granulocyte-macrophage colony-stimulating factor (GM-CSF), Type 2 interleukin-4 (IL-4) IL-5. To carry out detailed time-course analysis cellular changes bronchoalveolar lavage fluid (BAL), peripheral blood (PB), bone marrow (BM), aforementioned BAL serum, Balb/c...
Cigarette smoking is the main risk factor for development of chronic obstructive pulmonary disease (COPD), a major cause morbidity and mortality worldwide. Despite this, cellular molecular mechanisms that contribute to COPD pathogenesis are still poorly understood.The objective this study was assess IL-1 α β expression in patients investigate their respective roles perpetuating cigarette smoke-induced inflammation. Functional studies were pursued smoke-exposed mice using gene-deficient...
End-stage chronic obstructive pulmonary disease (COPD) is associated with an accumulation of lymphoid follicles. IL-17A implicated in COPD and neogenesis response to microbial stimuli. We hypothesized that increased peripheral lung tissue during end-stage also directly contributes cigarette smoke-induced neogenesis.To characterize the expression functional role COPD.Automated immune detection IL-17F was performed specimens collected from patients Global Initiative for Chronic Obstructive...
Rationale: Nontypeable Haemophilus influenzae (NTHi) causes acute exacerbation of chronic obstructive pulmonary disease (AECOPD). IL-17A is central for neutrophilic inflammation and has been linked to COPD pathogenesis.Objectives: We investigated whether elevated in NTHi-associated AECOPD required NTHi-exacerbated neutrophilia induced by cigarette smoke.Methods: Experimental studies with smoke NTHi infection were pursued gene-targeted mice using antibody intervention. was measured sputum...
Experimental models are critical for the understanding of lung health and disease indispensable drug development. However, pathogenetic clinical relevance is often unclear. Further, use animals in biomedical research controversial from an ethical perspective. The objective this task force was to issue a statement with recommendations about by facilitating in-depth discussions between respiratory scientists, provide overview literature on available models. Focus put their specific benefits...
We investigated the impact of cigarette smoke exposure on respiratory immune defense mechanisms. Mice were exposed to two cigarettes daily, 5 d/wk, for 2-4 mo. Tobacco decreased number dendritic cells (DCs) in lung tissue. Furthermore, dramatically reduced percentage B7.1-expressing DCs. Because DCs are believed be indispensable initiation adaptive responses, we responsiveness toward adenovirus. mo and inoculated with 2 x 10(8) pfu a replication-deficient adenovirus three occasions, wk...
The object of this study was to investigate the impact cigarette smoke on bacterial clearance and immune inflammatory parameters after infection with Pseudomonas aeruginosa in mice. We observed a delayed rate smoke-exposed compared sham-exposed This associated increased inflammation characterized by greater numbers neutrophils mononuclear cells bronchoalveolar lavage. After infection, we levels proinflammatory cytokines (tumor necrosis factor-alpha, interleukin-1beta, interleukin-6)...
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Abstract NK cells play essential roles in innate host defense against microbial infections and tumor surveillance. Although evidence suggests that smoking has adverse effects on the immune system, little is known about whether compromises cell effector functions. In this study, we show cigarette smoke-conditioned medium (SCM) dose-dependently inhibits vitro IFN-γ production by polyinosinic:polycytidylic acid (poly I:C)-activated PBMC isolated from nonsmoking individuals. Similarly, SCM...
Abstract Despite the presence of known mutagens and carcinogens in cigarette smoke, there is currently no evidence to show that smoking, or exposure can result heritable genetic mutation. We male mice exposed mainstream tobacco smoke (MTS) exhibit a significant increase germ-line mutation frequency spermatogonial stem cells. mature MTS for 6 12 weeks investigated mutations arising cells at expanded simple tandem repeat locus Ms6-hm. A generalized score test showed treatment effect (P =...
Alveolar macrophages (aMs) play a central role in respiratory host defense by sensing microbial antigens and initiating immune-inflammatory responses early the course of an infection. The purpose this study was to investigate effect cigarette smoke exposure on aMs after stimulation innate pattern recognition receptors (PRRs) murine model. To accomplish this, C57BL/6 mice were exposed for 8 weeks using two models exposure, nose-only or whole-body isolated from bronchoalveolar lavage. After...
Rationale: The pathogenesis of chronic obstructive pulmonary disease is associated with acute episodes bacterial exacerbations. most commonly isolated bacteria during exacerbation nontypeable Haemophilus influenzae (NTHI).Objectives: In this study, we investigated the in vivo consequences cigarette smoke exposure on inflammatory response to an NTHI challenge.Methods: C57BL/6 and BALB/c mice were exposed for 8 weeks subsequently challenged intranasally NTHI.Measurements Main Results: We...
The objective of this study was to characterize the impact cigarette smoke exposure on lung immune and inflammatory processes. BALB/c C57BL/6 mice were exposed for 4 days (acute) or at least 5 weeks (prolonged). Both mouse strains manifested an response after acute exposure, characterized by influx neutrophils mononuclear cells. Multiplex analysis revealed a greater than twofold increase cytokines IL-1alpha, -5, -6, -18, as well chemokines monocyte chemotactic protein-1 -3, macrophage...
Cigarette smoke is a documented reproductive toxicant associated with infertility and ovarian failure. However, the underlying mechanism(s) regulating toxic effects of cigarette are unknown. Therefore, we tested hypothesis that mainstream constituent, benzo[a]pyrene (BaP), induce apoptosis in follicles.Mice were exposed to ovaries analysed for follicle loss markers (TUNEL, Caspase 3, 8, Bax, Bcl-2, Fas FasL). Isolated from female pups cultured media containing increasing concentrations BaP...
Cigarette smoking among reproductive-aged women is increasing worldwide. a lifestyle behavior associated with important adverse health effects including subfertility and premature ovarian failure. We previously demonstrated that cigarette smoke (CS) exposure in mice decreases the primordial follicle pool; however, mechanism of action largely unknown. Therefore, present study was designed to elucidate mechanisms underlying CS exposure–induced loss. induced significant decrease relative weight...
Background Chronic obstructive pulmonary disease is a progressive lung that punctuated by periods of exacerbations (worsening symptoms) are attributable to viral infections. While rhinoviruses most commonly isolated viruses during episodes exacerbation, influenza have the potential become even more problematic with increased likelihood an epidemic. Methodology and Principal Findings This study examined impact current pharmacological targets namely systemic corticosteroid dexamethasone...
Cigarette smoking is a lifestyle behavior associated with significant adverse health effects, including subfertility and premature ovarian failure. smoke contains number of chemicals, many which are involved in the generation reactive oxygen species, can lead to apoptosis autophagy. Autophagy fundamental process that removes damaged organelles proteins through lysosomal degradation. The relevance autophagy toxicant-induced changes function largely unexplored. Previously, we reported exposure...
Overwhelming evidence links inflammation to the pathogenesis of smoking-related pulmonary diseases, especially chronic obstructive disease (COPD). Despite an increased understanding pathogenesis, mechanisms initiating smoking-induced inflammatory processes remain incompletely understood. To investigate that initiate and propagate smoke-induced inflammation, we used a well-characterised mouse model cigarette smoke exposure, mice deficient for interleukin (IL)-1α, IL-1β Toll-like receptor 4,...
It is currently not understood whether cigarette smoke exposure facilitates sensitisation to self-antigens and ensuing auto-reactive T cells drive chronic obstructive pulmonary disease (COPD)-associated pathologies. To address this question, mice were exposed for 2 weeks. Following a 2-week period of rest, challenged intratracheally with elastin 3 days or 1 month. Rag1 −/− , Mmp12 Il17a neutralising antibodies against active fragments used mechanistic investigations. Human...