Mechanisms underlying enhanced IgA production in Peyer's patch cells by membrane vesicles derived from Lactobacillus sakei

2021 ◽  
Author(s):  
Yuki Miyoshi ◽  
Azusa Saika ◽  
Takahiro Nagatake ◽  
Ayu Matsunaga ◽  
Jun Kunisawa ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Bone Marrow ◽  
Membrane Vesicle ◽  
Membrane Vesicles ◽  
Lactobacillus Sakei ◽  
Peyer’S Patch ◽  
Peyer's Patch ◽  
Iga Production ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Abstract We analyzed the mechanisms underlying enhanced IgA production in the cells of Peyer's patch cells via membrane vesicles derived from Lactobacillus sakei subsp. sakei NBRC 15893. Depletion of CD11c+ cells from Peyer's patch cells suppressed the enhanced IgA production mediated by membrane vesicles. Meanwhile, stimulation of bone marrow-derived dendritic cells with membrane vesicles increased gene expression of inducible nitric oxide synthase, retinaldehyde dehydrogenase 2, and several inflammatory cytokines. The production of nitric oxide and interleukin (IL)-6 by membrane vesicle stimulation was induced via Toll-like receptor 2 on bone marrow-derived dendritic cells. Inhibition of inducible nitric oxide synthase and retinaldehyde dehydrogenase 2, as well as neutralization of IL-6 in Peyer's patch cells, suppressed the enhanced IgA production by membrane vesicle stimulation. Hence, nitric oxide, retinoic acid, and IL-6 induced by MVs play crucial roles in the enhanced IgA production elicited by membrane vesicles in Peyer's patch cells.

scholarly journals Paraquat Modulates Immunological Function in Bone Marrow-Derived Macrophages

2021 ◽  
Author(s):  
Piyarat Srinont ◽  
Jaroon Wandee ◽  
Worapol Angwanich
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Bone Marrow ◽  
Cell Death ◽  
Cell Viability ◽  
Inducible Nitric Oxide Synthase ◽  
Ros Production ◽  
Oxygen Species ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Abstract Paraquat (PQ) is an herbicide commonly used worldwide. This herbicide is known to alter the human and animal immune systems. Many reports indicated that PQ impacts immune cell viability and functions. However, the underlying mechanism critical is still unknown. Therefore, the aim of this study was to evaluate effects of PQ on free radical production, oxidative stress, cell death, and pro-inflammatory gene expression of murine bone marrow-derived macrophages (BMDMs) from female C57BL/6NJcl mice in vitro. BMDMs were incubated with PQ at 0, 200, 400 µM for 24 h. Intracellular reactive oxygen species (ROS) production, apoptosis, cell viability, nitric oxide, inducible nitric oxide synthase (iNOS), and IL-6 expression of murine BMDMs were measured. The results revealed that PQ treatments led to decrease the cell viability and induced apoptotic cell death in a dose-dependent manner. Additionally, PQ induced reactive oxygen species (ROS) generation. The mRNA expression level of pro-inflammatory mediator gene IL-6 and inducible nitric oxide synthase (iNOS) were elevated, while the level of lipid peroxides (MDA) production was unaltered by PQ treatment. Interestingly, PQ led to a decrease in nitric oxide production depends on its concentration. These phenomena indicated that PQ increased cellular ROS production which induced apoptosis, and the herbicide triggers production of iNOS and IL-6 in murine BMDMs.

The role of SHIP1 in macrophage programming and activation

2004 ◽  
Vol 32 (5) ◽  
pp. 785-788 ◽  
Author(s):  
M.J. Rauh ◽  
L.M. Sly ◽  
J. Kalesnikoff ◽  
M.R. Hughes ◽  
L.-P. Cao ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Bone Marrow ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Endotoxin Tolerance ◽  
Negative Regulator ◽  
Collagen Formation ◽  
Phosphoinositide 3 Kinase ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

The SHIP1 (SH2-containing inositol-5′-phosphatase 1) acts as a negative regulator of proliferation, survival and end cell activation in haemopoietic cells. It does so, at least in part, by translocating to membranes after extracellular stimulation and hydrolysing the phosphoinositide 3-kinase-generated second messenger, PtdIns(3,4,5)P3 to PtdIns(3,4)P2. SHIP1−/− mice have, as a result, an increased number of neutrophils and monocyte/macrophages because their progenitors display enhanced survival and proliferation. These mice also suffer from osteoporosis because of an increased number of hyperactive osteoclasts and a significant neutrophil infiltration of the lungs. Interestingly, SHIP1−/− mice do not display endotoxin tolerance and we have found that lipopolysaccharide-induced endotoxin tolerance is contingent on up-regulating SHIP1, through the production of autocrine-acting transforming growth factor-β, in bone-marrow-derived macrophages and mast cells. Intriguingly, unlike bone-marrow-derived macrophages, SHIP1−/− peritoneal and alveolar macrophages produce 10-fold less NO than wild-type macrophages because these in vivo-generated macrophages have very high arginase I levels and this enzyme competes with inducible nitric oxide synthase for the substrate L-arginine. It is probable that, in the face of chronically increased PtdIns(3,4,5)P3 levels in their myeloid progenitors, SHIP1−/− mice display a skewed development away from M1 (killer) macrophages (which have high inducible nitric oxide synthase levels and produce NO to kill microorganisms and tumour cells), towards M2 (healing) macrophages (which have high arginase levels and produce ornithine to promote host-cell growth and collagen formation). This skewing probably occurs to avoid septic shock and suggests that the phosphoinositide 3-kinase pathway plays a critical role in programming macrophages.

Sign in / Sign up

Export Citation Format

Share Document