scholarly journals GI distress: A breath of fresh air in respiratory homeostasis

EBioMedicine ◽  
2019 ◽  
Vol 44 ◽  
pp. 12-13
Author(s):  
Richard Kinkead ◽  
Jean-Philippe Rousseau ◽  
Tara A. Janes
2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Sushila A. Toulmin ◽  
Chaitali Bhadiadra ◽  
Andrew J. Paris ◽  
Jeffrey H. Lin ◽  
Jeremy Katzen ◽  
...  

AbstractType II alveolar cells (AT2s) are critical for basic respiratory homeostasis and tissue repair after lung injury. Prior studies indicate that AT2s also express major histocompatibility complex class II (MHCII) molecules, but how MHCII expression by AT2s is regulated and how it contributes to host defense remain unclear. Here we show that AT2s express high levels of MHCII independent of conventional inflammatory stimuli, and that selective loss of MHCII from AT2s in mice results in modest worsening of respiratory virus disease following influenza and Sendai virus infections. We also find that AT2s exhibit MHCII presentation capacity that is substantially limited compared to professional antigen presenting cells. The combination of constitutive MHCII expression and restrained antigen presentation may position AT2s to contribute to lung adaptive immune responses in a measured fashion, without over-amplifying damaging inflammation.


2001 ◽  
Vol 90 (5) ◽  
pp. 1729-1735 ◽  
Author(s):  
Richard Kinkead ◽  
Lydie Dupenloup ◽  
Nadine Valois ◽  
Roumiana Gulemetova

To test the hypothesis that stress alters the performance of the respiratory control system, we compared the acute (20 min) responses to moderate hypoxia and hypercapnia of rats previously subjected to immobilization stress (90 min/day) with responses of control animals. Ventilatory measurements were performed on awake rats using whole body plethysmography. Under baseline conditions, there were no differences in minute ventilation between stressed and unstressed groups. Rats previously exposed to immobilization stress had a 45% lower ventilatory response to hypercapnia (inspiratory CO2 fraction = 0.05) than controls. In contrast, stress exposure had no statistically significant effect on the ventilatory response to hypoxia (inspiratory O2 fraction = 0.12). Stress-induced attenuation of the hypercapnic response was associated with reduced tidal volume and inspiratory flow increases; the frequency and timing components of the response were not different between groups. We conclude that previous exposure to a stressful condition that does not constitute a direct challenge to respiratory homeostasis can elicit persistent (≥24 h) functional plasticity in the ventilatory control system.


2015 ◽  
Vol 58 (3) ◽  
pp. 638-652 ◽  
Author(s):  
Amanda I. Gillespie ◽  
William Slivka ◽  
Charles W. Atwood ◽  
Katherine Verdolini Abbott

Purpose The larynx has a dual role in the regulation of gas flow into and out of the lungs while also establishing resistance required for vocal fold vibration. This study assessed reciprocal relations between phonatory functions—specifically, phonatory laryngeal airway resistance (R law )—and respiratory homeostasis during states of ventilatory gas perturbations. Method Twenty-four healthy women performed phonatory tasks while exposed to induced hypercapnia (high CO 2 ), hypocapnia (low CO 2 ), and normal breathing (eupnea). Effects of gas perturbations on R law were investigated as were the reciprocal effects of R law modulations on respiratory homeostasis. Results R law remained stable despite manipulations of inspired gas concentrations. In contrast, end-tidal CO 2 levels increased significantly during all phonatory tasks. Thus, for the conditions tested, R law did not adjust to accommodate ventilatory needs as predicted. Rather, stable R law was spontaneously accomplished at the cost of those needs. Conclusions Findings provide support for a theory of regulation wherein R law may be a control parameter in phonation. Results also provide insight into the influence of phonation on respiration. The work sets the foundation for future studies on laryngeal function during phonation in individuals with lower airway disease and other patient populations.


2013 ◽  
Vol 110 (19) ◽  
pp. E1788-E1796 ◽  
Author(s):  
G. Yuan ◽  
Y.-J. Peng ◽  
V. D. Reddy ◽  
V. V. Makarenko ◽  
J. Nanduri ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yael Segev ◽  
Haiat Nujedat ◽  
Eden Arazi ◽  
Mohammad H. Assadi ◽  
Ariel Tarasiuk

AbstractWhy obstructive sleep apnea (OSA) treatment does not completely restore healthy metabolic physiology is unclear. In rats, the need for respiratory homeostasis maintenance following airway obstruction (AO) is associated with a loss of thermoregulation and abnormal metabolic physiology that persists following successful obstruction removal. Here, we explored the effect of two different types of tracheal narrowing, i.e., AO and mild airway obstruction (mAO), and its removal on respiratory homeostasis and metabolic physiology. We show that after ten weeks, mAO vs. AO consumes sufficient energy that is required to maintain respiratory homeostasis and thermoregulation. Obstruction removal was associated with largely irreversible increased feeding associated with elevated serum ghrelin, hypothalamic growth hormone secretagogue receptor 1a, and a phosphorylated Akt/Akt ratio, despite normalization of breathing and energy requirements. Our study supports the need for lifestyle eating behavior management, in addition to endocrine support, in order to attain healthy metabolic physiology in OSA patients.


2009 ◽  
Vol 05 (01) ◽  
pp. 40
Author(s):  
Adam Yagui-Beltrán ◽  
Lisa M Coussens ◽  
David M Jablons ◽  
◽  
◽  
...  

Lung cancer is the leading cause of all cancer deaths in the US. The international scientific and clinical community has made significant advances toward understanding specific molecular mechanisms underlying lung carcinogenesis; however, despite these insights and advances in surgery and chemoradiotherapy, the prognosis for non-small-cell lung cancer (NSCLC) remains poor. Nonetheless, significant effort is being focused on advancing translational research evaluating the efficacy of novel targeted therapeutic strategies for lung cancer. Illustrative examples of this include antagonists of the epidermal growth factor receptor (EGFR), tyrosine kinase inhibitors (TKIs) such as gefitinib and erlotinib, and a diverse assortment of anti-angiogenic compounds targeting growth factors and/or their receptors that regulate tumorassociated angiogenic programs. In addition, with the increased awareness of the significant role chronically activated leukocytes play as potentiators of solid-tumor development, the role of innate and adaptive immune cells as regulators of lung carcinogenesis is being examined. While some of these studies are examining how novel therapeutic strategies may enhance the efficacy of lung cancer vaccines, others are evaluating the intrinsic characteristics of the immune response to lung cancer in order to identify rate-limiting molecular and/or cellular programs to target with novel anticancer therapeutics. In this article, we explore important aspects of the immune system and its role in regulating normal respiratory homeostasis compared with the immune response accompanying development of lung cancer. These hallmarks are then discussed in the context of recent efforts to develop lung cancer vaccines, where we have highlighted important concepts that must be taken into consideration for future development of novel therapeutic strategies and clinical trials assessing their efficacy.


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