Subclinical infection can be an initiator of inflammaging leading to degenerative disk disease: evidence from host-defense response mechanisms

Author(s):  
S. Rajasekaran ◽  
Tangavel Chitraa ◽  
S. Dilip Chand Raja ◽  
M. Raveendran ◽  
Nayagam Sharon Miracle ◽  
...  
CHEST Journal ◽  
1997 ◽  
Vol 112 (5) ◽  
pp. 1154-1158 ◽  
Author(s):  
G. Umberto Meduri

2012 ◽  
Vol 142 (5) ◽  
pp. S-859 ◽  
Author(s):  
Moiz A. Charania ◽  
Hamed Laroui ◽  
Hongchun Lui ◽  
Sarah A. Ingersoll ◽  
Saravanan Ayyadurai ◽  
...  

2017 ◽  
Vol 85 (4) ◽  
Author(s):  
Hua Yao ◽  
Hong Zhang ◽  
Kai Lan ◽  
Hong Wang ◽  
Yufeng Su ◽  
...  

ABSTRACT Insights into the host-microbial virulence factor interaction, especially the immune signaling mechanisms, could provide novel prevention and treatment options for pneumococcal diseases. Streptococcus pneumoniae endopeptidase O (PepO) is a newly discovered and ubiquitously expressed pneumococcal virulence protein. A PepO-mutant strain showed impaired adherence to and invasion of host cells compared with the isogenic wild-type strain. It is still unknown whether PepO is involved in the host defense response to pneumococcal infection. Here, we demonstrated that PepO could enhance phagocytosis of Streptococcus pneumoniae and Staphylococcus aureus by peritoneal exudate macrophages (PEMs). Further studies showed that PepO stimulation upregulated the expression of microRNA-155 (miR-155) in PEMs in a time- and dose-dependent manner. PepO-induced enhanced phagocytosis was decreased in cells transfected with an inhibitor of miR-155, while it was increased in cells transfected with a mimic of miR-155. We also revealed that PepO-induced upregulation of miR-155 in PEMs was mediated by Toll-like receptor 2 (TLR2)–NF-κB signaling and that the increased expression of miR-155 downregulated expression of SHIP1. Taken together, these results indicate that PepO induces upregulation of miR-155 in PEMs, contributing to enhanced phagocytosis and host defense response to pneumococci and Staphylococcus aureus.


2020 ◽  
Vol 11 ◽  
Author(s):  
Shuanglong Huang ◽  
Xuehua Zhang ◽  
W. G. Dilantha Fernando

A fundamental process culminating in the mechanisms of plant-pathogen interactions is the regulation of trophic divergence into biotrophic, hemibiotrophic, and necrotrophic interactions. Plant hormones, of almost all types, play significant roles in this regulatory apparatus. In plant-pathogen interactions, two classical mechanisms underlying hormone-dependent trophic divergence are long recognized. While salicylic acid dominates in the execution of host defense response against biotrophic and early-stage hemibiotrophic pathogens, jasmonic acid, and ethylene are key players facilitating host defense response against necrotrophic and later-stage hemibiotrophic pathogens. Evidence increasingly suggests that trophic divergence appears to be modulated by more complex signaling networks. Acting antagonistically or agonistically, other hormones such as auxins, cytokinins, abscisic acid, gibberellins, brassinosteroids, and strigolactones, as well as nitric oxide, are emerging candidates in the regulation of trophic divergence. In this review, the latest advances in the dynamic regulation of trophic divergence are summarized, emphasizing common and contrasting hormonal and nitric oxide signaling strategies deployed in plant-pathogen interactions.


Author(s):  
Naveen Jayapala ◽  
Navya Hulikunte Mallikarjunaiah ◽  
Hariprasad Puttaswamy ◽  
Hithamani Gavirangappa ◽  
Niranjana Siddapura Ramachandrappa

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