Differential expression of the CD14/TLR4 complex and inflammatory signaling molecules following i.c.v. administration of LPS

2006 ◽  
Vol 1095 (1) ◽  
pp. 85-95 ◽  
Author(s):  
Yun Xia ◽  
Kanato Yamagata ◽  
Teresa L. Krukoff
2021 ◽  
Vol 12 ◽  
Author(s):  
Austin Ferro ◽  
Yohan S. S. Auguste ◽  
Lucas Cheadle

Intercellular signaling molecules such as cytokines and their receptors enable immune cells to communicate with one another and their surrounding microenvironments. Emerging evidence suggests that the same signaling pathways that regulate inflammatory responses to injury and disease outside of the brain also play powerful roles in brain development, plasticity, and function. These observations raise the question of how the same signaling molecules can play such distinct roles in peripheral tissues compared to the central nervous system, a system previously thought to be largely protected from inflammatory signaling. Here, we review evidence that the specialized roles of immune signaling molecules such as cytokines in the brain are to a large extent shaped by neural activity, a key feature of the brain that reflects active communication between neurons at synapses. We discuss the known mechanisms through which microglia, the resident immune cells of the brain, respond to increases and decreases in activity by engaging classical inflammatory signaling cascades to assemble, remodel, and eliminate synapses across the lifespan. We integrate evidence from (1) in vivo imaging studies of microglia-neuron interactions, (2) developmental studies across multiple neural circuits, and (3) molecular studies of activity-dependent gene expression in microglia and neurons to highlight the specific roles of activity in defining immune pathway function in the brain. Given that the repurposing of signaling pathways across different tissues may be an important evolutionary strategy to overcome the limited size of the genome, understanding how cytokine function is established and maintained in the brain could lead to key insights into neurological health and disease.


2008 ◽  
Vol 146 (1-3) ◽  
pp. 157-168 ◽  
Author(s):  
Marie-Thérèse Bawolak ◽  
Karine Touzin ◽  
Marie Eve Moreau ◽  
Anik Désormeaux ◽  
Albert Adam ◽  
...  

2014 ◽  
Vol 92 (5) ◽  
pp. 321-328 ◽  
Author(s):  
William L. Patterson ◽  
Philippe T. Georgel

Chronic inflammation is a cyclical, self-stimulating process. Immune cells called to sites of inflammation release pro-inflammatory signaling molecules that stimulate activation of inducible enzymes and transcription factors. These enzymes and transcription factors then stimulate production of signaling molecules that attract more immune cells and induce more enzymatic and transcriptional activity, creating a perpetual loop of inflammation. This self-renewing pool of inflammatory stimuli makes for an ideal tumor microenvironment, and chronic inflammation has been linked to oncogenesis, tumor growth, tumor cell survival, and metastasis. Three protein pathways in particular, nuclear factor kappa B (NF-kB), cyclooxygenase (COX), and lipoxygenase (LOX), provide excellent examples of the cyclical, self-renewing nature of chronic inflammation-driven cancers. NF-kB is an inducible transcription factor responsible for the expression of a vast number of inflammation and cancer related genes. COX and LOX convert omega-6 (n-6) and omga-3 (n-3) polyunsaturated fatty acids (PUFA) into pro- and anti-inflammatory signaling molecules. These signaling molecules stimulate or repress activity of all three of these pathways. In this review, we will discuss the pro- and anti-inflammatory functions of these fatty acids and their role in chronic inflammation and cancer progression.


2006 ◽  
Vol 103 (9) ◽  
pp. 3322-3326 ◽  
Author(s):  
F. Weerkamp ◽  
M. R. M. Baert ◽  
B. A. E. Naber ◽  
E. E. L. Koster ◽  
E. F. E. de Haas ◽  
...  

Tumor Biology ◽  
2011 ◽  
Vol 32 (5) ◽  
pp. 1005-1012 ◽  
Author(s):  
Swati S. Jain ◽  
Manickaraj AshokKumar ◽  
Ranjana P. Bird

PLoS ONE ◽  
2020 ◽  
Vol 15 (10) ◽  
pp. e0233938
Author(s):  
Maitham A. Khajah ◽  
Ahmed Z. EL-Hashim ◽  
Khaled Y. Orabi ◽  
Sanaa Hawai ◽  
Hanan G. Sary

Physiology ◽  
2021 ◽  
Vol 36 (4) ◽  
pp. 235-245 ◽  
Author(s):  
James C. Poland ◽  
C. Robb Flynn

Bile acids (BAs) are a family of hydroxylated steroids secreted by the liver that aid in the breakdown and absorption of dietary fats. BAs also function as nutrient and inflammatory signaling molecules, acting through cognate receptors, to coordinate host metabolism. Commensal bacteria in the gastrointestinal tract are functional modifiers of the BA pool, affecting composition and abundance. Deconjugation of host BAs creates a molecular network that inextricably links gut microtia with their host. In this review we highlight the roles of BAs in mediating this mutualistic relationship with a focus on those events that impact host physiology and metabolism.


2017 ◽  
Vol 19 (suppl_6) ◽  
pp. vi55-vi55
Author(s):  
Khushboo Irshad ◽  
Chitrangda Srivastava ◽  
Nargis Malik ◽  
Chitra Sarkar ◽  
Deepak Gupta ◽  
...  

Author(s):  
R Villarreal-Calderon ◽  
J Palacios-Moreno ◽  
S Keefe ◽  
N Osnaya ◽  
R Torres-Jardon ◽  
...  

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