Multivalent gold nanoparticle–peptide conjugates for targeting intracellular bacterial infections

Nanoscale ◽  
2017 ◽  
Vol 9 (37) ◽  
pp. 14074-14093 ◽  
Author(s):  
Rimi Chowdhury ◽  
Humaira Ilyas ◽  
Anirban Ghosh ◽  
Haydar Ali ◽  
Arup Ghorai ◽  
...  

This study identifies and characterizes a gold nano-particle tagged antimicrobial peptide that can internalize cells and kill intracellular bacteria without being cytotoxic. It can also considerably reduceS.Typhi infection in animal model.

2020 ◽  
Author(s):  
Keqiang Chen ◽  
Teizo Yoshimura ◽  
Wanghua Gong ◽  
Cuimeng Tian ◽  
Jiaqiang Huang ◽  
...  

AbstractHost-derived antimicrobial peptides play an important role in the defense against extracellular bacterial infections. However, the capacity of antimicrobial peptides derived from macrophages as potential antibacterial effectors against intracellular pathogens remains unknown. In this study, we report that normal (wild type, WT) mouse macrophages increased their expression of the cathelicidin-related antimicrobial peptide (CRAMP) after infection by viable E. coli or stimulation with inactivated E. coli and its product LPS, a process involving activation of NF-κB followed by protease-dependent conversion of CRAMP from an inactive precursor to an active form. The active CRAMP was required by WT macrophages to eliminate phagocytosed E. coli, with participation of autophagy-related proteins ATG5, LC3-II, and LAMP-1 as well as conjugation of the bacteria with p62. The autophagy-mediated elimination of E. coli was impaired in CRAMP−/− macrophages resulting in retention of intracellular bacteria and fragmentation of macrophages. These results indicate CRAMP as a critical component in autophagy-mediated clearance of intracellular E. coli by macrophages.


2016 ◽  
Vol 17 (5) ◽  
pp. 613-619 ◽  
Author(s):  
Jlenia Brunetti ◽  
Chiara Falciani ◽  
Luisa Bracci ◽  
Alessandro Pini

2004 ◽  
Vol 17 (2) ◽  
pp. 348-369 ◽  
Author(s):  
Inés Colmegna ◽  
Raquel Cuchacovich ◽  
Luis R. Espinoza

SUMMARY Current evidence supports the concept that reactive arthritis (ReA) is an immune-mediated synovitis resulting from slow bacterial infections and showing intra-articular persistence of viable, nonculturable bacteria and/or immunogenetic bacterial antigens synthesized by metabolically active bacteria residing in the joint and/or elsewhere in the body. The mechanisms that lead to the development of ReA are complex and basically involve an interaction between an arthritogenic agent and a predisposed host. The way in which a host accommodates to invasive facultative intracellular bacteria is the key to the development of ReA. The details of the molecular pathways that explain the articular and extra-articular manifestations of the disease are still under investigation. Several studies have been done to gain a better understanding of the pathogenesis of ReA; these constitute the basis for a more rational therapeutic approach to this disease.


2021 ◽  
Vol 60 (1) ◽  
pp. 128-136
Author(s):  
Jaeyeong Park ◽  
Eunkyoung Shin ◽  
Ji-Hyun Yeom ◽  
Younkyung Choi ◽  
Minju Joo ◽  
...  

2019 ◽  
Vol 62 (4) ◽  
pp. 1875-1886 ◽  
Author(s):  
Kavita Yadav ◽  
Sandeep Kumar ◽  
Deepakkumar Mishra ◽  
Mohammad Asad ◽  
Madhurima Mitra ◽  
...  

2019 ◽  
Vol Volume 12 ◽  
pp. 2865-2874 ◽  
Author(s):  
Jialong Qi ◽  
Ruiyu Gao ◽  
Cunbao Liu ◽  
Bin Shan ◽  
Fulan Gao ◽  
...  

Blood ◽  
2002 ◽  
Vol 100 (10) ◽  
pp. 3703-3709 ◽  
Author(s):  
Annette Kolb-Mäurer ◽  
Martin Wilhelm ◽  
Florian Weissinger ◽  
Eva-Bettina Bröcker ◽  
Werner Goebel

Primitive hematopoietic stem cells (HSCs) in the bone marrow are rare pluripotent cells with the capacity to give rise to all lineages of blood cells. During commitment, progenitor cells are composed mainly of cells with the potential for differentiation into 1 or 2 lineages. This commitment involves the acquisition of specific growth factor receptors and the loss of others. Viral and bacterial infections may lead to profound disturbance of hematopoiesis, which is possibly due to different susceptibility of HSCs to infectious agents. Here, we show that quiescent human HSCs are fully resistant to infection by the intracellular bacteria, Listeria monocytogenes andSalmonella enterica serovariationtyphimurium, and the extracellular pathogen Yersinia enterocolitica. During myeloid/monocytic differentiation induced by incubation with stem cell factor, thrombopoietin, and flt-3 ligand, partially differentiated HSCs emerge, which readily take up these pathogens and also latex beads by macropinocytosis. After further monocytic differentiation, bacterial uptake by macropinocytosis still occurs but internalization of the pathogens is now mainly achieved by receptor-mediated phagocytosis. These results suggest that in the case of HSCs uptake mechanisms for bacteria develop sequentially.


2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Kelly E. Burns ◽  
Tanner P. McCleerey ◽  
Damien Thévenin

2014 ◽  
Vol 118 (19) ◽  
pp. 10302-10313 ◽  
Author(s):  
L. Gamrad ◽  
C. Rehbock ◽  
J. Krawinkel ◽  
B. Tumursukh ◽  
A. Heisterkamp ◽  
...  

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