scholarly journals Nitric Oxide–Releasing Nanoparticles Prevent Propionibacterium acnes– Induced Inflammation by Both Clearing the Organism and Inhibiting Microbial Stimulation of the Innate Immune Response

2015 ◽  
Vol 135 (11) ◽  
pp. 2723-2731 ◽  
Author(s):  
Min Qin ◽  
Angelo Landriscina ◽  
Jamie M. Rosen ◽  
Gabrielle Wei ◽  
Stephanie Kao ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Immune Response ◽  
Innate Immune Response ◽  
Propionibacterium Acnes ◽  
Innate Immune ◽  
Nitric Oxide Releasing ◽  
Stimulation Of

scholarly journals Innate immune response in bovine neutrophils stimulated with Mycoplasma bovis

2021 ◽  
Vol 52 (1) ◽  
Author(s):  
Satoshi Gondaira ◽  
Koji Nishi ◽  
Jumpei Fujiki ◽  
Hidetomo Iwano ◽  
Reina Watanabe ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Immune Response ◽  
Innate Immune Response ◽  
Quantitative Polymerase Chain Reaction ◽  
Polymerase Chain Reaction Analysis ◽  
Functional Expression ◽  
Innate Immune ◽  
Cytokine Gene Expression ◽  
Mycoplasma Bovis ◽  
Bovine Neutrophils

AbstractMycoplasma bovis (M. bovis) is a significant worldwide pathogen of cattle. Neutrophils have an important role in the innate immune response during infection with M. bovis. However, even though neutrophils accumulate in M. bovis infection, the interaction of M. bovis and neutrophils has not been fully elucidated. We attempted to elucidate the innate immune response of neutrophils stimulated with M. bovis and evaluate the transcriptome and functional analysis of bovine neutrophils stimulated with M. bovis. Proinflammatory cytokines, such as inducible nitric oxide (iNOS), which was the most increased gene in transcriptome analysis, were increased in quantitative polymerase chain reaction analysis of bovine neutrophils stimulated with live or heat-killed M. bovis. Nitric oxide and intracellular reactive oxygen species production of neutrophils stimulated with M. bovis was significantly increased. Neutrophils stimulated with M. bovis showed an increased ratio of nonapoptotic cell death compared to unstimulated controls. We demonstrated that neutrophil extracellular traps (NETs) formation was not recognized in neutrophils stimulated with live M. bovis. However, heat-killed M. bovis induced NETs formation. We also showed the interaction with M. bovis and bovine neutrophils regarding proinflammatory cytokine gene expression and functional expression related to NETs formation. Live and killed M. bovis induced innate immune responses in neutrophils and had the potential to induce NETs formation, but live M. bovis escaped NETs.

scholarly journals Exposure to artificial light at night alters innate immune response in wild great tit nestlings

2021 ◽  
Author(s):  
Ziegler Ann-Kathrin ◽  
Watson Hannah ◽  
Hegemann Arne ◽  
Meitern Richard ◽  
Canoine Virginie ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Immune Response ◽  
Immune Function ◽  
Innate Immune Response ◽  
Great Tit ◽  
Innate Immune ◽  
Artificial Light ◽  
Immune Challenge ◽  
Light At Night ◽  
Dark Night

The large-scale impact of urbanization on wildlife is rather well documented, however the mechanisms underlying the effects of urban environments on animal physiology and behaviour are still poorly understood. Here, we focused on one major urban pollutant - artificial light at night (ALAN) - and its effects on the capacity to mount an innate immune response in wild great tit Parus major nestlings. Exposure to ALAN alters circadian rhythms of physiological processes, by disrupting the nocturnal production of the hormone melatonin. Nestlings were exposed to a light source emitting 3 lux for seven consecutive nights. Subsequently, nestlings were immune-challenged with a lipopolysaccharide injection, and we measured haptoglobin and nitric oxide levels pre- and post-injection. Both haptoglobin and nitric oxide are important markers for innate immune function. We found that ALAN exposure altered the innate immune response, with ALAN nestlings having lower haptoglobin and higher nitric oxide levels after the immune-challenge compared to dark-night nestlings. Unexpectedly, nitric oxide levels were overall, lower after the immune-challenge than before. These effects were likely mediated by melatonin, since ALAN-treated birds had on average 49% lower melatonin levels than the dark-night birds. ALAN exposure did not have any clear effects on nestling growth. This study provides a potential physiological mechanism underlying the documented differences in immune function between urban and rural birds observed in other studies. Moreover, it gives evidence that ALAN exposure affects nestling physiology, potentially causing long-term effects on physiology and behaviour, which ultimately can affect their fitness.

scholarly journals TLR3-mediated NF-κB signaling in human esophageal epithelial cells

2009 ◽  
Vol 297 (6) ◽  
pp. G1172-G1180 ◽  
Author(s):  
Diana M. Lim ◽  
Sneha Narasimhan ◽  
Carmen Z. Michaylira ◽  
Mei-Lun Wang
Keyword(s):  
Immune Response ◽  
Epithelial Cells ◽  
Inflammatory Response ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Poly I:C ◽  
Esophageal Epithelium ◽  
Esophageal Epithelial Cells ◽  
Stimulation Of

Despite its position at the front line against ingested pathogens, very little is presently known about the role of the esophageal epithelium in host innate immune defense. As a key player in the innate immune response, Toll-like receptor (TLR) signaling has not been well characterized in human esophageal epithelial cells. In the present study, we investigated the inflammatory response and signaling pathways activated by TLR stimulation of human esophageal cells in vitro. Using quantitative RT-PCR, we profiled the expression pattern of human TLRs 1–10 in primary esophageal keratinocytes (EPC2), immortalized nontransformed esophageal keratinocytes (EPC2-hTERT), and normal human esophageal mucosal biopsies and found that TLRs 1, 2, 3, and 5 were expressed both in vivo and in vitro. Using the cytokine IL-8 as a physiological read out of the inflammatory response, we found that TLR3 is the most functional of the expressed TLRs in both primary and immortalized esophageal epithelial cell lines in response to its synthetic ligand polyinosinic polycytidylic acid [poly(I:C)]. Through reporter gene studies, we show that poly(I:C)-induced NF-κB activation is critical for the transactivation of the IL-8 promoter in vitro and that nuclear translocation of NF-κB occurs at an early time point following poly(I:C) stimulation of esophageal epithelial cells. Importantly, we also show that poly(I:C) stimulation induces the NF-κB-dependent esophageal epithelial expression of TLR2, leading to enhanced epithelial responsiveness of EPC2-hTERT cells to TLR2 ligand stimulation, suggesting an important regulatory role for TLR3-mediated NF-κB signaling in the innate immune response of esophageal epithelial cells. Our findings demonstrate for the first time that TLR3 is highly functional in the human esophageal epithelium and that TLR3-mediated NF-κB signaling may play an important regulatory role in esophageal epithelial homeostasis.

Sequence-dependent stimulation of the mammalian innate immune response by synthetic siRNA

2005 ◽  
Vol 23 (4) ◽  
pp. 457-462 ◽  
Author(s):  
Adam D Judge ◽  
Vandana Sood ◽  
Janet R Shaw ◽  
Dianne Fang ◽  
Kevin McClintock ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Sequence Dependent ◽  
Stimulation Of
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