SP-A and TLR4 localization in lung tissue of SM-exposed patients.

Autor: Ghaffarpour S; Immunoregulation Research Center, Shahed University, Tehran, Iran., Foroutan A; Department of Physiology, Shaheed Beheshti University of Medical Sciences, Tehran, Iran. Electronic address: sa.foroutan@sbu.ac.ir., Askari N; Department of Biology, Faculty of Basic Sciences, Shahid Bahonar, University of Kerman, Kerman, Iran., Abbas FM; Department of Oral & Maxillofacial Pathology, School of Dentistry, Shahid Beheshti University of Medical Sciences, Tehran, Iran., Salehi E; Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran., Nikoonejad M; Immunoregulation Research Center, Shahed University, Tehran, Iran., Naghizadeh MM; Immunoregulation Research Center, Shahed University, Tehran, Iran; Non Communicable Diseases Research Center, Fasa University of Medical Science, Fasa, Iran., Eskandarian M; Department of Immunology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran., Moghadam KG; Internal Medicine Department, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: kgohari@tums.ac.ir., Akbari HMH; Department of Pathology, Shahid Beheshti University of Medical Sciences, Tehran, Iran; Traditional Medicine School, Tehran University of Medical Sciences, Tehran, Iran., Yarmohammadi ME; Department of Otolaryngology, Shahed University, Tehran, Iran., Ghazanfari T; Immunoregulation Research Center, Shahed University, Tehran, Iran; Department of Immunology, Shahed University, Tehran, Iran. Electronic address: ghazanfari@shahed.ac.ir.
Jazyk: angličtina
Zdroj: International immunopharmacology [Int Immunopharmacol] 2020 Mar; Vol. 80, pp. 105936. Date of Electronic Publication: 2019 Nov 11.
DOI: 10.1016/j.intimp.2019.105936
Abstrakt: Introduction: Long-term pulmonary complications are one of the major long-term consequences of sulfur mustard (SM) exposure. Toll-like receptor 4 (TLR4) involves in the pathogenesis of several pulmonary disorders. Surfactant protein-A (SP-A) regulates LPS-induced TLR4 localization and activation responses. However, the intensity and significance of TLR4 and SP-A expression by lung cells in SM-exposed patients is not clear.
Methods: The gene expression of TLR4 (through real-time PCR) and TLR4 and SP-A positive cells and alveolar type II cells, as SP-A producers, (using IHC) were assessed in formalin fixed paraffin embedded (FFPE) specimens from SM-exposed (n = 17), and non-SM exposed individuals (n = 12).
Results: TLR4 gene expression did not change between study groups. However, its cell surface presentation was significantly reduced in SM-exposed patients and particularly in which with constrictive bronchiolitis compared with the control group (P < 0.001 and P = 0.002, respectively). Frequency of alveolar type II cells was lower in the case group rather than the control group while the number of SP-A positive cells did not alter.
Conclusions: These findings suggest that reduced TLR4 cell surface presentation may have anti-inflammatory function and SP-A may have a critical role in regulation of inflammatory responses in SM-exposed patients. Further investigation on other possible mechanisms involved in TLR4 internalization maybe help to illustrate the modulatory or inflammatory activity of TLR4 in these patients.
Competing Interests: Declaration of Competing Interest All of the authors declare no conflict of interest.
(Copyright © 2019. Published by Elsevier B.V.)
Databáze: MEDLINE