scholarly journals Airways inflammatory and atopy-related responses in athletes

2006 ◽  
Vol 18 (2) ◽  
pp. 46
Author(s):  
AJ McKune ◽  
LL Smith

The prevalence of asthma and airway hyperresponsiveness (AHR) in highly trained endurance athletes is rising. The type of training (i.e. endurance, or speed and power) seems to influence the airway symptoms. High-intensity exercise and training might contribute to the development of asthma or AHR in athletes previously unaffected by these airway disorders. Repeated hyperventilation of unconditioned air, as well as air containing irritants and/or allergens has been suggested to cause thermal, mechanical, or osmotic airway trauma resulting in damage to the airway epithelium. Subsequent airway inflammatory responses may be responsible for the development of atopy-related symptoms in endurance athletes such as those observed in asthma and AHR. Eosinophils and neutrophils are the inflammatory cells that have been frequently observed to be elevated in the airways of endurance athletes. The trafficking of these cells to the airways may possibly be regulated by TH2 cytokines that are expressed in the airways in response to epithelial cell damage. In addition, these airway inflammatory responses may lead to airway remodelling similar to that which occurs in asthma. The effect of the exercise challenge itself may initiate airway atopy-related and inflammatory responses in endurance athletes. While the literature seems to support the role of local airway conditions and/or events in inducing atopy-related symptoms in athletes, it is proposed that alterations in the hormonal and/or cytokine milieu with intense competition and/or training may also play a role. South African Journal of Sports Medicine Vol. 18 (2) 2006: pp. 46-51

2009 ◽  
Vol 18 (2) ◽  
pp. 46 ◽  
Author(s):  
AJ McKune ◽  
LL Smith

The prevalence of asthma and airway hyperresponsiveness (AHR) in highly trained endurance athletes is rising. The type of training (i.e. endurance, or speed and power) seems to influence the airway symptoms. High-intensity exercise and training might contribute to the development of asthma or AHR in athletes previously unaffected by these airway disorders. Repeated hyperventilation of unconditioned air, as well as air containing irritants and/or allergens has been suggested to cause thermal, mechanical, or osmotic airway trauma resulting in damage to the airway epithelium. Subsequent airway inflammatory responses may be responsible for the development of atopy-related symptoms in endurance athletes such as those observed in asthma and AHR. Eosinophils and neutrophils are the inflammatory cells that have been frequently observed to be elevated in the airways of endurance athletes. The trafficking of these cells to the airways may possibly be regulated by TH2 cytokines that are expressed in the airways in response to epithelial cell damage. In addition, these airway inflammatory responses may lead to airway remodelling similar to that which occurs in asthma. The effect of the exercise challenge itself may initiate airway atopy-related and inflammatory responses in endurance athletes. While the literature seems to support the role of local airway conditions and/or events in inducing atopy-related symptoms in athletes, it is proposed that alterations in the hormonal and/or cytokine milieu with intense competition and/or training may also play a role. South African Journal of Sports Medicine Vol. 18 (2) 2006: pp. 46-51


2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Tao Yu ◽  
Young-Su Yi ◽  
Yanyan Yang ◽  
Jueun Oh ◽  
Deok Jeong ◽  
...  

Inflammation is a complex biological response of tissues to harmful stimuli such as pathogens, cell damage, or irritants. Inflammation is considered to be a major cause of most chronic diseases, especially in more than 100 types of inflammatory diseases which include Alzheimer's disease, rheumatoid arthritis, asthma, atherosclerosis, Crohn's disease, colitis, dermatitis, hepatitis, and Parkinson's disease. Recently, an increasing number of studies have focused on inflammatory diseases. TBK1 is a serine/threonine-protein kinase which regulates antiviral defense, host-virus interaction, and immunity. It is ubiquitously expressed in mouse stomach, colon, thymus, and liver. Interestingly, high levels of active TBK1 have also been found to be associated with inflammatory diseases, indicating that TBK1 is closely related to inflammatory responses. Even though relatively few studies have addressed the functional roles of TBK1 relating to inflammation, this paper discusses some recent findings that support the critical role of TBK1 in inflammatory diseases and underlie the necessity of trials to develop useful remedies or therapeutics that target TBK1 for the treatment of inflammatory diseases.


2014 ◽  
Vol 6 (1) ◽  
Author(s):  
Agnieszka Gajos ◽  
Sławomir Kujawski ◽  
Małgorzata Gajos ◽  
Żaneta Chatys ◽  
Piotr Bogacki

Summary Study aim: discussion of applications of H-reflex in kinesiology. Material and methods: used keywords H-reflex, Hoffmann reflex, kinesiology, EMG, biomechanics, orthopaedics, rehabilitation, and sports medicine to search EBSCO database. Used subsequent results to analyse clinical trials and to review articles. Results: in many studies, authors describe the role of examining H-reflex in biomechanics, orthopaedics, rehabilitation, and sports medicine. Conclusions: the H-reflex seems to be useful for examining progress in orthopaedic and physiotherapy treatment, as well as for analysing aspects of biomechanics. However, it seems that the H-reflex has limitations as a tool for examining training progress in strength athletes, and is not the most efficient in endurance athletes.


Parasitology ◽  
2007 ◽  
Vol 134 (6) ◽  
pp. 789-796 ◽  
Author(s):  
A. B. M. da SILVEIRA ◽  
S. J. ADAD ◽  
R. CORREA-OLIVEIRA ◽  
J. B. FURNESS ◽  
D. D'AVILA REIS

SUMMARYThe mechanisms involved in the pathogenesis of chagasic megacolon are not completely characterized. Although autoimmunity may play a role in the pathogenesis of Chagas' disease, recent studies suggest a positive association of tissue parasitism, inflammation, and severity of lesions. The aim of this study was to evaluate the role of inflammatory cells and the occurrence of fibrosis in the colon of chagasic patients with and without megacolon. Samples from 26 patients were randomly selected and paraffin-embedded tissue blocks were sectioned and evaluated by histology and immunohistochemistry to analyse the occurrence and relation among eosinophils, mast cells, macrophages and fibrosis. Section analyses showed that the presence of eosinophils and mast cells in the analysed inflammatory cells has a direct correlation with fibrosis density in the chagasic megacolon. These data suggest that the megacolon's pathogenesis is based on a continuous process of cell damage. Our data propose that eosinophils, mast cells and macrophages may have a direct connection with the occurrence of fibrosis in the colon of chagasic patients. We believe that potential therapeutic agents against these cells could avoid the fibrosis process and contribute to prevent the development of chagasic megacolon.


Cancers ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1337
Author(s):  
Federica Raggi ◽  
Maria Bosco

Inflammatory cells are major players in the onset of cancer. The degree of inflammation and type of inflammatory cells in the tumor microenvironment (TME) are responsible for tilting the balance between tumor progression and regression. Cancer-related inflammation has also been shown to influence the efficacy of conventional therapy. Mononuclear phagocytes (MPs) represent a major component of the inflammatory circuit that promotes tumor progression. Despite their potential to activate immunosurveillance and exert anti-tumor responses, MPs are subverted by the tumor to support its growth, immune evasion, and spread. MP responses in the TME are dictated by a network of stimuli integrated through the cross-talk between activatory and inhibitory receptors. Alterations in receptor expression/signaling can create excessive inflammation and, when chronic, promote tumorigenesis. Research advances have led to the development of new therapeutic strategies aimed at receptor targeting to induce a tumor-infiltrating MP switch from a cancer-supportive toward an anti-tumor phenotype, demonstrating efficacy in different human cancers. This review provides an overview of the role of MP receptors in inflammation-mediated carcinogenesis and discusses the most recent updates regarding their targeting for immunotherapeutic purposes. We focus in particular on the TREM-1 receptor, a major amplifier of MP inflammatory responses, highlighting its relevance in the development and progression of several types of inflammation-associated malignancies and the promises of its inhibition for cancer immunotherapy.


2019 ◽  
Vol 20 (17) ◽  
pp. 4091 ◽  
Author(s):  
Mar Carrión ◽  
Klaus W. Frommer ◽  
Selene Pérez-García ◽  
Ulf Müller-Ladner ◽  
Rosa P. Gomariz ◽  
...  

Rheumatic diseases encompass a diverse group of chronic disorders that commonly affect musculoskeletal structures. Osteoarthritis (OA) and rheumatoid arthritis (RA) are the two most common, leading to considerable functional limitations and irreversible disability when patients are unsuccessfully treated. Although the specific causes of many rheumatic conditions remain unknown, it is generally accepted that immune mechanisms and/or uncontrolled inflammatory responses are involved in their etiology and symptomatology. In this regard, the bidirectional communication between neuroendocrine and immune system has been demonstrated to provide a homeostatic network that is involved in several pathological conditions. Adipokines represent a wide variety of bioactive, immune and inflammatory mediators mainly released by adipocytes that act as signal molecules in the neuroendocrine-immune interactions. Adipokines can also be synthesized by synoviocytes, osteoclasts, osteoblasts, chondrocytes and inflammatory cells in the joint microenvironment, showing potent modulatory properties on different effector cells in OA and RA pathogenesis. Effects of adiponectin, leptin, resistin and visfatin on local and systemic inflammation are broadly described. However, more recently, other adipokines, such as progranulin, chemerin, lipocalin-2, vaspin, omentin-1 and nesfatin, have been recognized to display immunomodulatory actions in rheumatic diseases. This review highlights the latest relevant findings on the role of the adipokine network in the pathophysiology of OA and RA.


2007 ◽  
Vol 19 (2) ◽  
pp. 52 ◽  
Author(s):  
SC Rose ◽  
HA Chipps ◽  
EM Peters

Background and objectives. Little is known of the fluid replacement habits of participants in mountain bike (MTB) endurance events. This survey set out to determine the current perceptions and practices of this group of endurance athletes. Method. Four hundred and twelve participants in the 3- day 2006 Sani2C (MTB) race completed questionnaires that elicited information regarding their regular fluid intake practices during competitive MTB endurance events. This included their general approach to fluid replacement, their fluid intake practices (type, amount and frequency), urine output and hydration status. Results. While 70% (N = 290) reported that they based their fluid intake practices on personal past experiences, less than half the group (N = 177, 43%) were aware of official sport-specific guidelines. Although 86% (N = 354) reported making use of commercially available sport-specific drinks, consumption of water alone was reported by 34% of respondents (N = 140). The majority (N = 225, 55%) of the mountain bikers reported drinking every 16 - 30 minutes during an endurance ride, while 35% (N = 144) reported drinking every 0 - 15 minutes. Fifty-three per cent (N = 182) of the male respondents and 45% (N = 23) of female respondents reported a routine intake of ≥ 750 ml per hour during endurance rides. This included 2 women who reported regular intakes of between 1 500 and 2 000 ml/hr. Only 7 (2%) reported receiving medical care for dehydration following their participation in previous MTB rides. Conclusions. This survey indicates that although more than half of the mountain bikers did not acknowledge specific awareness of the official fluid replacement guidelines, over 80% reported drinking regularly during a race, and 52% (N = 212) reported a usual intake of ≥ 750 ml/hr during endurance races. Until scientific studies have carefully examined the hydration status and fluid replacement needs of mountain bikers, MTB cyclists are cautioned against the practice of over-hydrating. South African Journal of Sports Medicine Vol. 19 (2) 2007: pp. 52-58


2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Apoorva Pandey ◽  
Ritu Kulshrestha ◽  
Surendra Kumar Bansal

Abstract Background Pulmonary fibrosis (PF) is a progressive and lethal lung disease of elderly whose incidence has been increasing following the Covid-19 pandemic caused by severe acute respiratory syndrome corona virus 2 (SARS-CoV-2). PF immunopathogenesis involves progressive alveolar epithelial cell damage, release of damage-associated molecular patterns (DAMPs), and extracellular matrix (ECM) injury. We assessed the dynamic role of LMW-hyaluronan (LMW-HA) as DAMP in initiation of host immune TLR-2,4 responses and as determinant in progression of ECM injury to fibrosis. Male Wistar rats were divided into Group I (saline control, n = 24) and Group II (intratracheal bleomycin, 7 U/kg/animal, n = 24). Animals were euthanized on 0, 7, 14, and 28 days. The time course of release of LMW-HA, TLR-2,4 mRNA and protein levels, and NF-κB-p65 levels after bleomycin injury were correlated with the development of parenchymal inflammation, remodelling, and fibrosis. Results Acute lung injury caused by bleomycin significantly increases the pro-inflammatory LMW-HA levels and elevates TLR-2,4 levels on day 7. Subsequently, TLR-2 upregulation, TLR-4 downregulation, and NF-κB signalling follow on days 14 and 28. This results in progressive tissue inflammation, alveolar and interstitial macrophage accumulation, and fibrosis. Conclusions LMW-HA significantly increases in PF caused by non-infectious and infectious (Covid-19) etiologies. The accumulating HA fragments function as endogenous DAMPs and trigger inflammatory responses, through differential TLR2 and TLR4 signalling, thus promoting inflammation and macrophage influx. LMW-HA are reflective of the state of ongoing tissue inflammation and may be considered as a natural biosensor for fibrotic lung diseases and as potential therapeutic targets.


Cells ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 2338
Author(s):  
Yijie Hu ◽  
Leon Chi ◽  
Wolfgang M Kuebler ◽  
Neil M Goldenberg

Perivascular inflammation is a prominent pathologic feature in most animal models of pulmonary hypertension (PH) as well as in pulmonary arterial hypertension (PAH) patients. Accumulating evidence suggests a functional role of perivascular inflammation in the initiation and/or progression of PAH and pulmonary vascular remodeling. High levels of cytokines, chemokines, and inflammatory mediators can be detected in PAH patients and correlate with clinical outcome. Similarly, multiple immune cells, including neutrophils, macrophages, dendritic cells, mast cells, T lymphocytes, and B lymphocytes characteristically accumulate around pulmonary vessels in PAH. Concomitantly, vascular and parenchymal cells including endothelial cells, smooth muscle cells, and fibroblasts change their phenotype, resulting in altered sensitivity to inflammatory triggers and their enhanced capacity to stage inflammatory responses themselves, as well as the active secretion of cytokines and chemokines. The growing recognition of the interaction between inflammatory cells, vascular cells, and inflammatory mediators may provide important clues for the development of novel, safe, and effective immunotargeted therapies in PAH.


2019 ◽  
Vol 20 (17) ◽  
pp. 4170 ◽  
Author(s):  
Yue Gao ◽  
Zhengying Bian ◽  
Wenyao Xue ◽  
Qianwen Li ◽  
Yu Zeng ◽  
...  

Interleukin (IL)-23 is considered an effective therapeutic target for the treatment of psoriasis because of the crucial role of the IL-23/IL-17 axis in the pathogenesis of psoriasis, and it has recently been reported to be involved in ILC3 cell differentiation. In this study, we report that eukaryotically expressed rhIL23R-CHR/Fc, as an endogenous extracellular receptor analogue, could be a natural antagonist in an imiquimod (IMQ)-induced psoriasis-like mouse model, including the antagonizing effect of suppressed inflammation in the skin lesion, decreased production of pro-inflammatory cells, and reduced the expression of pro-inflammatory factors. The rhIL23R-CHR/Fc fusion protein inhibits both innate immune and adaptive immune-mediated inflammatory responses. These findings shed light on rhIL23R-CHR/Fc as a promising candidate therapy for the treatment of psoriasis.


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