scholarly journals Dermal adipocytes protect against invasive Staphylococcus aureus skin infection

Science ◽  
2015 ◽  
Vol 347 (6217) ◽  
pp. 67-71 ◽  
Author(s):  
Ling-juan Zhang ◽  
Christian F. Guerrero-Juarez ◽  
Tissa Hata ◽  
Sagar P. Bapat ◽  
Raul Ramos ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Antimicrobial Peptide ◽  
Host Defense ◽  
Bacterial Growth ◽  
Skin Infection ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Defense Function ◽  
Host Defense Function

Adipocytes have been suggested to be immunologically active, but their role in host defense is unclear. We observed rapid proliferation of preadipocytes and expansion of the dermal fat layer after infection of the skin by Staphylococcus aureus. Impaired adipogenesis resulted in increased infection as seen in Zfp423nur12 mice or in mice given inhibitors of peroxisome proliferator–activated receptor γ. This host defense function was mediated through the production of cathelicidin antimicrobial peptide from adipocytes because cathelicidin expression was decreased by inhibition of adipogenesis, and adipocytes from Camp−/− mice lost the capacity to inhibit bacterial growth. Together, these findings show that the production of an antimicrobial peptide by adipocytes is an important element for protection against S. aureus infection of the skin.

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.

scholarly journals Attenuation of host defense function of lung phagocytes in young cystic fibrosis patients

2006 ◽  
Vol 5 (1) ◽  
pp. 17-25 ◽  
Author(s):  
Neil E. Alexis ◽  
Marianne S. Muhlebach ◽  
David B. Peden ◽  
Terry L. Noah
Keyword(s):  
Cystic Fibrosis ◽  
Host Defense ◽  
Defense Function ◽  
Host Defense Function

scholarly journals Operative indication for esophageal cancer patients from a view point of host defense function.

1987 ◽  
Vol 20 (10) ◽  
pp. 2421-2426
Author(s):  
Takao SAITO ◽  
Kenji ZEZE ◽  
Akihiko KUWAHARA ◽  
Masaki MIYAHARA ◽  
Katsuhiro SHIMODA ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Cancer Patients ◽  
Host Defense ◽  
View Point ◽  
Operative Indication ◽  
Defense Function ◽  
Host Defense Function

scholarly journals Post-treatment with the PPAR-γ agonist pioglitazone inhibits inflammation and bacterial growth during Klebsiella pneumonia

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Ivan Ramirez-Moral ◽  
Bianca Lima Ferreira ◽  
Alex F. de Vos ◽  
Tom van der Poll
Keyword(s):  
Klebsiella Pneumoniae ◽  
Bacterial Growth ◽  
Virulent Strain ◽  
Respiratory Pathogen ◽  
Klebsiella Pneumonia ◽  
Peroxisome Proliferator ◽  
Bacterial Clearance ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ppar Γ ◽  
Highly Virulent

AbstractAgonists of peroxisome proliferator-activated receptor (PPAR)-γ have been suggested as potential adjuvant therapy in bacterial pneumonia because of their capacity to inhibit inflammation and enhance bacterial clearance. Previous studies only assessed the effects of pretreatment with these compounds, thereby bearing less relevance for the clinical scenario. Moreover, PPAR-γ agonists have not been studied in pneumonia caused by Klebsiella pneumoniae, a common human respiratory pathogen of which antibiotic treatment is hampered by increasing antimicrobial resistance. Here we show that administration of the PPAR-γ agonist pioglitazone 6 or 8 h after infection of mice with a highly virulent strain of Klebsiella pneumoniae via the airways results in reduced cytokine and myeloperoxidase levels in the lungs at 24 h after infection, as well as reduced bacterial growth in the lungs and decreased dissemination to distant organs at 42 h post-infection. These results suggest that pioglitazone may be an interesting agent in the treatment of Klebsiella pneumonia.

scholarly journals Peroxisome proliferator-activated receptor agonist rosiglitazone improves host defense against Pseudomonas aeruginosa in a murine model of pneumonia

Critical Care ◽  
2013 ◽  
Vol 17 (Suppl 4) ◽  
pp. P111
Author(s):  
Crisitina Nagae ◽  
Cassiano Gonçalves-de-Albuquerque ◽  
Alessandra Ferreira ◽  
Raysa Captivo ◽  
Larissa Camisão ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Host Defense ◽  
Murine Model ◽  
Receptor Agonist ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor

scholarly journals Pathogen induction of CXCR4/TLR2 cross-talk impairs host defense function

2008 ◽  
Vol 105 (36) ◽  
pp. 13532-13537 ◽  
Author(s):  
G. Hajishengallis ◽  
M. Wang ◽  
S. Liang ◽  
M. Triantafilou ◽  
K. Triantafilou
Keyword(s):  
Host Defense ◽  
Cross Talk ◽  
Pathogen Induction ◽  
Defense Function ◽  
Host Defense Function
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