Alterations of the Host Defense Mechanism in Burned Patients

1987 ◽  
Vol 67 (1) ◽  
pp. 47-56 ◽  
Author(s):  
Kevin Moran ◽  
Andrew M. Munster
2018 ◽  
Vol 218 (9) ◽  
pp. 1424-1435 ◽  
Author(s):  
Alessandra di Masi ◽  
Loris Leboffe ◽  
Fabio Polticelli ◽  
Federica Tonon ◽  
Cristina Zennaro ◽  
...  

2019 ◽  
Vol 51 (12) ◽  
pp. 1-10 ◽  
Author(s):  
Yi Sak Kim ◽  
Prashanta Silwal ◽  
Soo Yeon Kim ◽  
Tamotsu Yoshimori ◽  
Eun-Kyeong Jo

AbstractMycobacterium tuberculosis (Mtb) is a major causal pathogen of human tuberculosis (TB), which is a serious health burden worldwide. The demand for the development of an innovative therapeutic strategy to treat TB is high due to drug-resistant forms of TB. Autophagy is a cell-autonomous host defense mechanism by which intracytoplasmic cargos can be delivered and then destroyed in lysosomes. Previous studies have reported that autophagy-activating agents and small molecules may be beneficial in restricting intracellular Mtb infection, even with multidrug-resistant Mtb strains. Recent studies have revealed the essential roles of host nuclear receptors (NRs) in the activation of the host defense through antibacterial autophagy against Mtb infection. In particular, we discuss the function of estrogen-related receptor (ERR) α and peroxisome proliferator-activated receptor (PPAR) α in autophagy regulation to improve host defenses against Mtb infection. Despite promising findings relating to the antitubercular effects of various agents, our understanding of the molecular mechanism by which autophagy-activating agents suppress intracellular Mtb in vitro and in vivo is lacking. An improved understanding of the antibacterial autophagic mechanisms in the innate host defense will eventually lead to the development of new therapeutic strategies for human TB.


Hematology ◽  
2009 ◽  
Vol 2009 (1) ◽  
pp. 255-258 ◽  
Author(s):  
Bruce Furie

Abstract The hemostatic process is a host defense mechanism to preserve the integrity of the closed high pressure circulatory system. This process must remain inactive but poised to minimize extravasation of blood from the vasculature following tissue injury. Given the complexity of the hemostatic mechanism, paradigms developed from biochemical and cell biological approaches have been revisited by studying thrombus formation in a live animal by intravital microscopy. Many of these paradigms have proven accurate, but others need to be reconsidered given the results of whole animal experiments.


2003 ◽  
Vol 125 (6) ◽  
pp. 1613-1625 ◽  
Author(s):  
Koji Hase ◽  
Masamoto Murakami ◽  
Mitsutoshi Iimura ◽  
Sheri P Cole ◽  
Yoshimune Horibe ◽  
...  

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