scholarly journals Role of human neutrophil peptides in the initial interaction between lung epithelial cells and CD4+lymphocytes

2007 ◽  
Vol 81 (4) ◽  
pp. 1022-1031 ◽  
Author(s):  
Rosanna Vaschetto ◽  
Jonathan Grinstein ◽  
Lorenzo Del Sorbo ◽  
Aye Aye Khine ◽  
Stefanos Voglis ◽  
...  
2016 ◽  
Vol 8 (17) ◽  
pp. 2017-2031 ◽  
Author(s):  
Simona Panella ◽  
Maria Elena Marcocci ◽  
Ignacio Celestino ◽  
Sergio Valente ◽  
Clemens Zwergel ◽  
...  

Author(s):  
Dinesh Devadoss ◽  
Shashi P. Singh ◽  
Arpan Acharya ◽  
Kieu Chinh Do ◽  
Palsamy Periyasamy ◽  
...  

BackgroundThe role of lung epithelial cells in HIV-1-related lung comorbidities remains unclear, and the major hurdle in curing HIV is the persistence of latent HIV reservoirs in people living with HIV (PLWH). The advent of combined antiretroviral therapy has considerably increased the life span; however, the incidence of chronic lung diseases is significantly higher among PLWH. Lung epithelial cells orchestrate the respiratory immune responses and whether these cells are productively infected by HIV-1 is debatable.MethodsNormal human bronchial epithelial cells (NHBEs) grown on air–liquid interface were infected with X4-tropic HIV-1LAV and examined for latency using latency-reversing agents (LRAs). The role of CD4 and CXCR4 HIV coreceptors in NHBEs were tested, and DNA sequencing analysis was used to analyze the genomic integration of HIV proviral genes, Alu-HIVgag-pol, HIV-nef, and HIV-LTR. Lung epithelial sections from HIV-infected humans and SHIV-infected macaques were analyzed by FISH for HIV-gag-pol RNA and epithelial cell-specific immunostaining.Results and DiscussionNHBEs express CD4 and CXCR4 at higher levels than A549 cells. NHBEs are infected with HIV-1 basolaterally, but not apically, by X4-tropic HIV-1LAV in a CXCR4/CD4-dependent manner leading to HIV-p24 antigen production; however, NHBEs are induced to express CCR5 by IL-13 treatment. In the presence of cART, HIV-1 induces latency and integration of HIV provirus in the cellular DNA, which is rescued by the LRAs (endotoxin/vorinostat). Furthermore, lung epithelial cells from HIV-infected humans and SHIV-infected macaques contain HIV-specific RNA transcripts. Thus, lung epithelial cells are targeted by HIV-1 and could serve as potential HIV reservoirs that may contribute to the respiratory comorbidities in PLWH.


2015 ◽  
Vol 73 (7) ◽  
pp. ftv045 ◽  
Author(s):  
Cristiane Alcantara ◽  
Paloma Korehisa Maza ◽  
Bianca Carla Silva Campitelli Barros ◽  
Erika Suzuki

Development ◽  
1989 ◽  
Vol 105 (2) ◽  
pp. 263-270 ◽  
Author(s):  
Y. Hirai ◽  
A. Nose ◽  
S. Kobayashi ◽  
M. Takeichi

The role of Ca2+-dependent cell-cell adhesion molecules, E- and P-cadherins, in the histogenesis of mouse embryonic lung was studied. All epithelial cells of the lung express both E- and P-cadherin at the early developmental stage. P-cadherin, however, gradually disappears during development, initially from the main bronchi and eventually from all epithelial cells. When a monoclonal antibody to E-cadherin (ECCD-1) was added to monolayer cultures of lung epithelial cells, it induced a partial disruption of their cell-cell adhesion, while a monoclonal antibody to P-cadherin (PCD-1) showed a subtle effect. A mixture of the two antibodies, however, displayed a synergistic effect. We then tested the effect of the antibodies on the morphogenesis of lung primordia using an organ culture system. In control media, the explants formed typical bronchial trees. In the presence of ECCD-1, the explants grew up at the same rate as in the control, but their morphogenesis was affected. The control explants formed round epithelial lobules with an open luminal space at the tips of the bronchial trees, whereas the lobules of explants incubated with ECCD-1 tended to be flat and devoid of the luminal space. PCD-1 showed a similar but very small effect. A mixture of the two antibodies, however, showed a stronger effect: the branching of epithelia was partially suppressed and the arrangement of epithelial cells was distorted in many places. These results suggest that E- and P-cadherin have a synergistic role in the organization of epithelial cells in lung morphogenesis.


2008 ◽  
Vol 67 (5) ◽  
pp. 448-452 ◽  
Author(s):  
B. Rivas-Santiago ◽  
J. C. L. Contreras ◽  
E. Sada ◽  
R. Hernández-Pando

2011 ◽  
Vol 177 (3) ◽  
pp. 241-246 ◽  
Author(s):  
Li Bai ◽  
Zubin Yu ◽  
Changzheng Wang ◽  
Guisheng Qian ◽  
Guansong Wang

2021 ◽  
Author(s):  
Sara Lenart ◽  
Peter Lenart ◽  
Hana Kotasova ◽  
Vendula Pelkova ◽  
Veronika Sedlakova ◽  
...  

TACSTD2 encodes a transmembrane glycoprotein Trop2 commonly overexpressed in carcinomas. While the Trop2 protein was discovered already in 1981 and first antibody-drug conjugate targeting Trop2 were recently approved cancer therapy, the physiological role of Trop2 is still not fully understood. In this article, we show that TACSTD2/Trop2 expression is evolutionarily conserved in lungs of various vertebrates. By analysis of publicly available transcriptomic data we demonstrate that TACSTD2 level consistently increases in lungs infected with miscellaneous pathogens. Single cell and subpopulation based transcriptomic data revealed that the major source of TACSTD2 transcript are lung epithelial cells and their progenitors and that TACSTD2 is induced directly in lung epithelial cells following infection. This increase may represent a mechanism to maintain/restore epithelial barrier function and contribute to regeneration process in infected/damaged lungs.


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