Phagocytosis and the microtubule cytoskeleton

2002 ◽  
Vol 80 (5) ◽  
pp. 509-515 ◽  
Author(s):  
Rene E Harrison ◽  
Sergio Grinstein
Keyword(s):  
Host Defense ◽  
Defense Mechanism ◽  
Fc Receptor ◽  
Signaling Proteins ◽  
Microtubule Cytoskeleton ◽  
Complex Sequence ◽  
Sequence Of Events ◽  
Host Defense Mechanism

Phagocytosis is a critical host defense mechanism used by macrophages and neutrophils to clear invading pathogens. The complex sequence of events resulting in internalization and degradation of the pathogens is a coordinated process involving lipids, signaling proteins, and the cytoskeleton. Here, we examine the role of the microtubule cytoskeleton in supporting both the engulfment of pathogens and their elimination within phagolysosomes.Key words: macrophage, microtubule, phagocytosis, maturation, Fc receptor.

Possible role of macrophages induced by an irridoid glycoside (RLJ-NE-299A) in host defense mechanism

2011 ◽  
Vol 11 (1) ◽  
pp. 128-135 ◽  
Author(s):  
Tabasum Sidiq ◽  
Anamika Khajuria ◽  
Pankaj Suden ◽  
Rohit Sharma ◽  
Surjeet Singh ◽  
...  
Keyword(s):  
Host Defense ◽  
Defense Mechanism ◽  
Host Defense Mechanism

Role of tumor-infiltrating lymphocytes in the host defense mechanism against lung cancer

1988 ◽  
Vol 38 (4) ◽  
pp. 221-226 ◽  
Author(s):  
Kosei Yasumoto ◽  
Sadanori Takeo ◽  
Tokujiro Yano ◽  
Hisashi Nakahashi ◽  
Akira Nagashima ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Host Defense ◽  
Defense Mechanism ◽  
Tumor Infiltrating Lymphocytes ◽  
Host Defense Mechanism ◽  
Infiltrating Lymphocytes

scholarly journals Dram1 confers resistance to Salmonella infection

2021 ◽  
Author(s):  
Samrah Masud ◽  
Rui Zhang ◽  
Tomasz K. Prajsnar ◽  
Annemarie H. Meijer
Keyword(s):  
Defense Mechanism ◽  
Early Response ◽  
Protective Role ◽  
Infection Model ◽  
Transgenic Zebrafish ◽  
Functional Link ◽  
Morpholino Knockdown ◽  
Host Defense Mechanism ◽  
Important Host

Dram1 is a stress and infection inducible autophagy modulator that functions downstream of transcription factors p53 and NFκB. Using a zebrafish embryo infection model, we have previously shown that Dram1 provides protection against the intracellular pathogen Mycobacterium marinum by promoting the p62-dependent xenophagy of bacteria that have escaped into the cytosol. However, the possible interplay between Dram1 and other anti-bacterial autophagic mechanisms remains unknown. Recently, LC3-associated phagocytosis (LAP) has emerged as an important host defense mechanism that requires components of the autophagy machinery and targets bacteria directly in phagosomes. Our previous work established LAP as the main autophagic mechanism by which macrophages restrict growth of Salmonella Typhimurium in a systemically infected zebrafish host. We therefore employed this infection model to investigate the possible role of Dram1 in LAP. Morpholino knockdown or CRISPR/Cas9-mediated mutation of Dram1 led to reduced host survival and increased bacterial burden during S. Typhimurium infections. In contrast, overexpression of dram1 by mRNA injection curtailed Salmonella replication and reduced mortality of the infected host. During the early response to infection, GFP-Lc3 levels in transgenic zebrafish larvae correlated with the dram1 expression level, showing over two-fold reduction of GFP-Lc3-Salmonella association in dram1 knockdown or mutant embryos and an approximately 30% increase by dram1 overexpression. Since LAP is known to require the activity of the phagosomal NADPH oxidase, we used a Salmonella biosensor strain to detect bacterial exposure to reactive oxygen species (ROS) and found that the ROS response was largely abolished in the absence of dram1. Together, these results demonstrate the host protective role of Dram1 during S. Typhimurium infection and suggest a functional link between Dram1 and the induction of LAP.

scholarly journals Human Serum Albumin Is an Essential Component of the Host Defense Mechanism Against Clostridium difficile Intoxication

2018 ◽  
Vol 218 (9) ◽  
pp. 1424-1435 ◽  
Author(s):  
Alessandra di Masi ◽  
Loris Leboffe ◽  
Fabio Polticelli ◽  
Federica Tonon ◽  
Cristina Zennaro ◽  
...  
Keyword(s):  
Clostridium Difficile ◽  
Human Serum Albumin ◽  
Serum Albumin ◽  
Human Serum ◽  
Host Defense ◽  
Defense Mechanism ◽  
Essential Component ◽  
Host Defense Mechanism

scholarly journals Mitofusin 2-Deficiency Suppresses Mycobacterium tuberculosis Survival in Macrophages

Cells ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 1355 ◽  
Author(s):  
Junghwan Lee ◽  
Ji-Ae Choi ◽  
Soo-Na Cho ◽  
Sang-Hun Son ◽  
Chang-Hwa Song
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Molecular Mechanisms ◽  
Defense Mechanism ◽  
Mitochondrial Fission ◽  
Mycobacterial Infection ◽  
Mitofusin 2 ◽  
Unstimulated Control ◽  
Host Defense Mechanism ◽  
Important Host

Apoptosis is an important host defense mechanism against mycobacterial infection. However, the molecular mechanisms regulating apoptosis during mycobacterial infection are not well known. Recent reports suggest that bacterial infection regulates mitochondrial fusion and fission in various ways. Here, we investigated the role of mitochondria in Mycobacterium tuberculosis (Mtb)-infected macrophages. Mtb H37Rv (Rv) infection induced mitofusin 2 (MFN2) degradation, leading to mitochondrial fission. Interestingly, Mtb H37Ra (Ra) infection induced significantly greater mitochondrial fragmentation than Rv infection. Mtb-mediated Parkin, an E3 ubiquitin ligase, contributed to the degradation of MFN2. To evaluate the role of endoplasmic reticulum stress in the production of Parkin during Mtb infection, we analyzed Parkin production in 4-phenylbutyric acid (4-PBA)-pretreated macrophages. Pretreatment with 4-PBA reduced Parkin production in Mtb-infected macrophages. In contrast, the level of MFN2 production recovered to a level similar to that of the unstimulated control. In addition, Ra-infected macrophages had reduced mitochondrial membrane potential (MMP) compared to those infected with Rv. Interestingly, intracellular survival of mycobacteria was decreased in siMFN2-transfected macrophages; in contrast, overexpression of MFN2 in macrophages increased Mtb growth compared with the control.

scholarly journals Autophagy-activating strategies to promote innate defense against mycobacteria

2019 ◽  
Vol 51 (12) ◽  
pp. 1-10 ◽  
Author(s):  
Yi Sak Kim ◽  
Prashanta Silwal ◽  
Soo Yeon Kim ◽  
Tamotsu Yoshimori ◽  
Eun-Kyeong Jo
Keyword(s):  
Host Defense ◽  
Defense Mechanism ◽  
Multidrug Resistant ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Innate Defense ◽  
Host Defense Mechanism ◽  
A Cell

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.

Sign in / Sign up

Export Citation Format

Share Document