scholarly journals The translational repressor T-cell intracellular antigen-1 (TIA-1) is a key modulator of Th2 and Th17 responses driving pulmonary inflammation induced by exposure to house dust mite

2012 ◽  
Vol 146 (1-2) ◽  
pp. 8-14 ◽  
Author(s):  
Maria Simarro ◽  
Giorgio Giannattasio ◽  
Wei Xing ◽  
Emma-Maria Lundequist ◽  
Samantha Stewart ◽  
...  
Keyword(s):  
T Cell ◽  
House Dust ◽  
House Dust Mite ◽  
Pulmonary Inflammation ◽  
Translational Repressor ◽  
Dust Mite ◽  
Intracellular Antigen

scholarly journals Effect of Low-Level Laser Therapy (LLLT) in Pulmonary Inflammation in Asthma Induced by House Dust Mite (HDM): Dosimetry Study

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Nicole Cristine Rigonato-Oliveira ◽  
Auriléia Aparecida de Brito ◽  
Luana Beatriz Vitoretti ◽  
Gabriel de Cunha Moraes ◽  
Tawany Gonçalves ◽  
...  
Keyword(s):  
Chronic Inflammation ◽  
Laser Therapy ◽  
House Dust ◽  
House Dust Mite ◽  
Structural Parameters ◽  
Pulmonary Inflammation ◽  
Low Level Laser Therapy ◽  
Low Level Laser ◽  
Level Laser ◽  
Dust Mite

Asthma is characterized by chronic inflammation in the airways. Several models have been proposed for the discovery of new therapies. Low-Level Laser Therapy (LLLT) is relatively new and effective, very low cost, with no side effects. However, there is still no consensus on the optimal dose to be used. In this sense, the objective of the present study was to evaluate the best dose in an experimental model of asthma induced by House Dust Mite (HDM). Balb/c mice received administration of 100 ug/animal HDM and LLLT applications (diode laser: 660 nm, 100 mW and four different energies 1J, 3J, 5J, and 7.5J) for 16 days. After 24 hours, we studied inflammatory, functional, and structural parameters. The results showed that LBI was able to modulate the pulmonary inflammation observed by reducing the number of cells in Bronchoalveolar Lavage Fluid (BALF) as well as reducing the percentage of neutrophils, eosinophils and T lymphocytes. On the other hand, LLLT increased the level of IL-10 and reduced levels of IL-4, IL-5 and IL-13 in BALF. LLLT was able to reduce the production of mucus, peribronchial eosinophils, collagen deposition, bronchoconstriction index, and bronchial and muscular thickening in the airways. We concluded that the use of LLLT in the treatment of chronic inflammation of the airways attenuated the inflammatory process and functional and structural parameters. We emphasize, in general, that the 1J and 3J laser presented better results. Thus, photobiomodulation may be considered a promising tool for the treatment of chronic pulmonary allergic inflammation observed in asthma.

scholarly journals G Protein-Coupled Receptor Kinase 2 (GRK2) Regulates T Cell Response in a Murine Model of House Dust Mite-Induced Asthma

2021 ◽  
Vol 2 ◽  
Author(s):  
Ananth K. Kammala ◽  
Canchai Yang ◽  
Reynold A. Panettieri ◽  
Rupali Das ◽  
Hariharan Subramanian
Keyword(s):  
T Cell ◽  
Mouse Model ◽  
G Protein ◽  
House Dust ◽  
House Dust Mite ◽  
T Cell Response ◽  
Receptor Kinase ◽  
G Protein Coupled Receptor ◽  
Dust Mite ◽  
G Protein Coupled

G protein-coupled receptor kinase 2 (GRK2) is an adapter protein that modulates G protein-coupled receptor (GPCR) signaling. It also regulates the functions and activity of other intracellular proteins in many cell types. Accordingly, GRK2 is thought to contribute to disease progression by a variety of mechanisms related to its multifunctional roles. Indeed, GRK2 levels are enhanced in patient samples as well as in preclinical models of several diseases. We have previously shown that GRK2 regulates mast cell functions, and thereby contributes to exacerbated inflammation during allergic reactions. In the current study, we observed that GRK2 levels are enhanced in the lungs of human asthma patients and in mice sensitized to house dust mite extract (HDME) allergen. Consistent with these findings, interleukin (IL)-4 and IL-13 levels were reduced in the lungs of GRK2+/− mice in a HMDE mouse model of asthma. Because Th2 cells are the major source of these cytokines during asthma, we determined the role of GRK2 in regulating T cell-specific responses in our HMDE mouse model. We observed a significant reduction of airway hyperresponsiveness (AHR), lung eosinophil and lymphocyte counts, serum IgE, Th2 cytokines (IL-4 and IL-13), goblet cell hyperplasia and mucus production in mice that had reduced GRK2 expression specifically in T cells. Collectively, our studies reveal an important role for GRK2 in regulating T cell response during asthma pathogenesis and further elucidation of the mechanisms through which GRK2 modulates airway inflammation will lead to the development of new therapeutic strategies for asthma.

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