Next Article in Journal
89Zr, a Radiometal Nuclide with High Potential for Molecular Imaging with PET: Chemistry, Applications and Remaining Challenges
Previous Article in Journal
Isoferulic Acid, a New Anti-Glycation Agent, Inhibits Fructose- and Glucose-Mediated Protein Glycation in Vitro
Molecules 2013, 18(6), 6455-6468; doi:10.3390/molecules18066455
Article

Bioactive Secondary Metabolites of a Marine Bacillus sp. Inhibit Superoxide Generation and Elastase Release in Human Neutrophils by Blocking Formyl Peptide Receptor 1

1,2,3
, 4
, 3
, 5
, 3
, 3
 and 3,6,*
1 Department of Anesthesiology, Taipei Veterans General Hospital, Taipei 112, Taiwan 2 Graduate Institute of Clinical Medical Sciences, College of Medicine, Chang Gung University, Taoyuan 333, Taiwan 3 Graduate Institute of Natural Products, College of Medicine, Chang Gung University, Taoyuan 333, Taiwan 4 Department of Cosmetic Science, and Research Center for Industry of Human Ecology, Chang Gung University of Science and Technology, Taoyuan 333, Taiwan 5 National Museum of Marine Biology & Aquarium, Pingtung 944, Taiwan 6 Chinese Herbal Medicine Research Team, Healthy Aging Research Center, Chang Gung University, Taoyuan 333, Taiwan
* Author to whom correspondence should be addressed.
Received: 25 April 2013 / Revised: 28 May 2013 / Accepted: 30 May 2013 / Published: 3 June 2013
(This article belongs to the Section Metabolites)
Download PDF [1551 KB, 18 June 2014; original version 18 June 2014]

Abstract

It is well known that overwhelming neutrophil activation is closely related to acute and chronic inflammatory injuries. Formyl peptide receptor 1 (FPR1) plays an important role in activation of neutrophils and may represent a potent therapeutic target in inflammatory diseases. In the present study, we demonstrated that IA-LBI07-1 (IA), an extract of bioactive secondary metabolites from a marine Bacillus sp., has anti-inflammatory effects in human neutrophils. IA significantly inhibited superoxide generation and elastase release in formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP)-activated neutrophils, but failed to suppress the cell responses activated by non-FPR1 agonists. IA did not alter superoxide production and elastase activity in cell-free systems. IA also attenuated the downstream signaling from FPR1, such as the Ca2+, MAP kinases and AKT pathways. In addition, IA inhibited the binding of N-formyl-Nle-Leu-Phe-Nle-Tyr-Lys-fluorescein, a fluorescent analogue of FMLP, to FPR1 in human neutrophils and FPR1-transfected HEK293 cells. Taken together, these results show that the anti-inflammatory effects of IA in human neutrophils are through the inhibition of FPR1. Also, our data suggest that IA may have therapeutic potential to decrease tissue damage induced by human neutrophils.
Keywords: elastase; formyl peptide receptor; Bacillus sp.; neutrophil; superoxide elastase; formyl peptide receptor; Bacillus sp.; neutrophil; superoxide
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Share & Cite This Article

Export to BibTeX |
EndNote


MDPI and ACS Style

Yang, S.-C.; Lin, C.-F.; Chang, W.-Y.; Kuo, J.; Huang, Y.-T.; Chung, P.-J.; Hwang, T.-L. Bioactive Secondary Metabolites of a Marine Bacillus sp. Inhibit Superoxide Generation and Elastase Release in Human Neutrophils by Blocking Formyl Peptide Receptor 1. Molecules 2013, 18, 6455-6468.

View more citation formats

Related Articles

Article Metrics

Comments

Citing Articles

[Return to top]
Molecules EISSN 1420-3049 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert