Mediators on Human Airway Smooth Muscle

Armour, Carol; Johnson, Patricia A.; Anticevich, S. Z.; Ammit, Alaina J.; McKay, Karen; Hughes, Margaret; Black, Judith L.

doi:10.1111/j.1440-1681.1997.tb01818.x

Cited by 18 publications

(8 citation statements)

References 23 publications

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“…In addition to the increased presence of immunoregulatory cells, asthmatics experience structural airway remodeling including increases in size and number of mucoussecreting globular cells and variable increases in wall thickness (19). Additionally, smooth muscle hyperplasia may occur in the airways increasing the smooth muscle area by up to three times (6). Inflammation and remodeling of the airways contribute to bronchial hyperresponsiveness, an exaggeration of the bronchoconstrictor response to pathogens or other stimuli contacting the airway epithelium (26).…”

Section: Asthmamentioning

confidence: 99%

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Effects of an acute bout of moderate-intensity exercise on postprandial lipemia and airway inflammation

Johnson

Kurti

Smith

et al. 2016

Appl. Physiol. Nutr. Metab.

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Obesity and asthma often coexist in the same people. Both are characterized by the presence of low-grade systemic inflammation. A high-fat diet may contribute to concurrent development of both conditions by promoting a pro-inflammatory postprandial environment leading to a transient accumulation of blood lipids (postprandial lipemia; PPL) and acute airway inflammation. Previous results from our lab have shown an ~20% increase in airway inflammation two hours after consuming a high-fat meal (HFM) that was significantly associated with increased plasma triglycerides. While acute exercise has been shown to attenuate PPL, it is unknown whether these protective effects will translate to reduced airway inflammation after a high-fat meal. PURPOSE: To determine the effects of an acute bout of exercise on airway inflammation after a HFM. We tested the hypothesis that an acute bout of exercise 12 hours before a high-fat meal would protect against subsequent airway inflammation in healthy men and would be related to the decreased PPL and systemic inflammatory markers. METHODS: In a randomized cross-over study, 12 healthy college-aged men consumed a HFM (1g fat/1kg body weight) 12 hours following exercise (EX; 60 min at 60% VO2max) or without exercise (CON).Exhaled nitric oxide (eNO; measure of airway inflammation), blood lipid profiles (venous sample; total cholesterol, HDL, LDL, triglycerides, glucose), inflammatory markers (hsCRP, TNF-α, IL-6) and pulmonary function tests (PFT) (forced expiratory volume in 1-s,forced vital capacity, forced expiratory flow at 25-75% of vital capacity) were measured pre-HFM, two hours, and four hours post-HFM. RESULTS: Baseline eNO was not different (p>0.05) between trials. eNO increased (p<0.05) post HFM at two hours in the both CON and EX conditions. eNO between trials was not different (p>0.05). Triglycerides were significantly increased two and four hours post HFM but were not different (p>0.05) between conditions. There was no relationship (p>0.05) between eNO and triglycerides or systemic inflammatory markers for any time point in either condition. Pulmonary function did not differ (p>0.05) between any condition.CONCLUSION: These results demonstrate that an acute bout of moderate intensity exercise 12 hours before a HFM does not attenuate postprandial airway inflammation or lipemia in healthy college-aged men.v

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Section: Asthmamentioning

confidence: 99%

“…Inflammation and remodeling of the airways contribute to bronchial hyperresponsiveness, an exaggeration of the bronchoconstrictor response to pathogens or other stimuli contacting the airway epithelium (26). Together, airway inflammation, remodeling, hyperresponsiveness, and possible airway edema contribute to overall airway narrowing (6,19).…”

Section: Asthmamentioning

confidence: 99%

Effects of an acute bout of moderate-intensity exercise on postprandial lipemia and airway inflammation

Johnson

Kurti

Smith

et al. 2016

Appl. Physiol. Nutr. Metab.

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“…A irway smooth muscle (ASM) 3 cells are key determinants of asthma due to their ability to contract in response to inflammatory cell products (1,2). Due to intrinsic phenotype plasticity, airway myocytes exhibit a capacity for multifunctional behavior and contribute to local inflammation and fibrosis (3).…”

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confidence: 99%

IL-17A Induces Eotaxin-1/CC Chemokine Ligand 11 Expression in Human Airway Smooth Muscle Cells: Role of MAPK (Erk1/2, JNK, and p38) Pathways

Rahman¹,

Yamasaki

Yang³

et al. 2006

The Journal of Immunology

120

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Recently, IL-17A has been shown to be expressed in higher levels in respiratory secretions from asthmatics and correlated with airway hyperresponsiveness. Although these studies raise the possibility that IL-17A may influence allergic disease, the mechanisms remain unknown. In this study, we investigated the molecular mechanisms involved in IL-17A-mediated CC chemokine (eotaxin-1/CCL11) production from human airway smooth muscle (ASM) cells. We found that incubation of human ASM cells with rIL-17A resulted in a significant increase of eotaxin-1/CCL11 release from ASM cells that was reduced by neutralizing anti-IL-17A mAb. Moreover, IL-17A significantly induced eotaxin-1/CCL11 release and mRNA expression, an effect that was abrogated with cycloheximide and actinomycin D treatment. Furthermore, transfection studies using a luciferase-driven reporter construct containing eotaxin-1/CCL11 proximal promoter showed that IL-17A induced eotaxin-1/CCL11 at the transcriptional level. IL-17A also enhanced significantly IL-1β-mediated eotaxin-1/CCL11 mRNA, protein release, and promoter activity in ASM cells. Primary human ASM cells pretreated with inhibitors of MAPK p38, p42/p44 ERK, JNK, or JAK but not PI3K, showed a significant decrease in eotaxin-1/CCL11 release upon IL-17A treatment. In addition, IL-17A mediated rapid phosphorylation of MAPK (p38, JNK, and p42/44 ERK) and STAT-3 but not STAT-6 or STAT-5 in ASM cells. Taken together, our data provide the first evidence of IL-17A-induced eotaxin-1/CCL11 expression in ASM cells via MAPK (p38, p42/p44 ERK, JNK) signaling pathways. Our results raise the possibility that IL-17A may play a role in allergic asthma by inducing eotaxin-1/CCL11 production.

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“…We assessed the potential role of 8‐epi‐PGF 2 α in cholinergic responsiveness by adding a subthreshold concentration in the organ bath prior to constructing a dose–response curve to ACh. As it has been shown that the addition of inflammatory mediators to the organ bath solution increases the responsiveness to ACh of isolated bronchial rings from healthy humans (Jongejan et al ., 1990; Armour et al ., 1997), it was speculated that 8‐epi‐PGF 2 α would act in a similar way in equine bronchi. But neither in healthy nor in heaves‐affected horses was the response (E max and pD 2 ) to ACh enhanced by addition of 8‐epi‐PGF 2 α (Table 2).…”

Section: Discussionmentioning

confidence: 99%

Effects of 8‐epi‐PGF₂_αon isolated bronchial smooth muscle of healthy and heaves‐affected horses

Kirschvink¹,

Art²,

Lekeux³

et al. 2001

Vet Pharm & Therapeutics

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8-Epi-PGF2alpha, a prostaglandin-like compound generated by oxidative stress, has been shown to be an in vitro bronchoconstrictor in airways from healthy laboratory animals and healthy humans, but it has never been studied in diseased airways. Here, the bronchoconstrictive capacity of 8-epi-PGF2alpha on isolated bronchial rings (BR) of healthy and heaves-affected horses was evaluated by comparing the maximal effect and the potency of 8-epi-PGF2alpha to those of (1) acetylcholine (ACh), (2) its stereoisomer PGF2alpha and (3) its synthetic receptor agonist, U46619. Furthermore, the potential capacity of 8-epi-PGF2alpha to enhance the cholinergic (ACh) responsiveness of bronchial smooth muscle was investigated. 8-Epi-PGF2alpha contracted BR with a rank order of efficacy of Ach > U44619 > PGF2alpha > 8-epi-PGF2alpha in both healthy and heaves-affected horses. The contractile maximal response elicited by 8-epi-PGF2alpha was significantly smaller than that elicited by the other drugs, but was significantly higher in BR from heaves-affected horses than in those sampled in healthy horses, whilst pD2 values were similar. A subthreshold concentration of 8-epi-PGF2alpha (10-7 M) did not induce in vitro cholinergic hyper-responsiveness in BR of either healthy or heaves-affected horses. In conclusion, it has been demonstrated that 8-epi-PGF2alpha is an in vitro bronchoconstrictor of minor importance in healthy horses, but whose efficacy is significantly increased in heaves-affected horses.

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Mediators on Human Airway Smooth Muscle

Cited by 18 publications

References 23 publications

Effects of an acute bout of moderate-intensity exercise on postprandial lipemia and airway inflammation

Effects of an acute bout of moderate-intensity exercise on postprandial lipemia and airway inflammation

IL-17A Induces Eotaxin-1/CC Chemokine Ligand 11 Expression in Human Airway Smooth Muscle Cells: Role of MAPK (Erk1/2, JNK, and p38) Pathways

Effects of 8‐epi‐PGF₂_αon isolated bronchial smooth muscle of healthy and heaves‐affected horses

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Mediators on Human Airway Smooth Muscle

Cited by 18 publications

References 23 publications

Effects of an acute bout of moderate-intensity exercise on postprandial lipemia and airway inflammation

Effects of an acute bout of moderate-intensity exercise on postprandial lipemia and airway inflammation

IL-17A Induces Eotaxin-1/CC Chemokine Ligand 11 Expression in Human Airway Smooth Muscle Cells: Role of MAPK (Erk1/2, JNK, and p38) Pathways

Effects of 8‐epi‐PGF2αon isolated bronchial smooth muscle of healthy and heaves‐affected horses

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Effects of 8‐epi‐PGF₂_αon isolated bronchial smooth muscle of healthy and heaves‐affected horses