Novel mechanism of C‐reactive protein for enhancing mouse liver innate immunity†

Inatsu, Akihito; Kinoshita, Manabu; Nakashima, Hiroyuki; Shimizu, Jun; Saitoh, Daizoh; Tamai, Susumu; Seki, Shu

doi:10.1002/hep.22888

Cited by 56 publications

(63 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our recent studies have revealed that gadolinium chloride (GdCl 3 ), which reportedly depletes Kupffer cells or inhibits their functions, suppresses lipopolysaccharide (LPS)-induced superoxide production but augments TNF production [1]. In addition, C-reactive protein (CRP) augments phagocytosis by Kupffer cells but suppresses their TNF-producing capability [2]. We also recently reported that GdCl 3 pretreatment completely inhibited concanavalin-Ainduced hepatitis by decreasing superoxide-producing CD68 + Kupffer cells without suppression of serum TNF levels [3].…”

Section: Introductionmentioning

confidence: 98%

Characterization of two F4/80-positive Kupffer cell subsets by their function and phenotype in mice

Kinoshita

Uchida

Sato

et al. 2010

Journal of Hepatology

Self Cite

253

255

View full text Add to dashboard Cite

Section: Introductionmentioning

confidence: 98%

Characterization of two F4/80-positive Kupffer cell subsets by their function and phenotype in mice

Kinoshita

Uchida

Sato

et al. 2010

Journal of Hepatology

Self Cite

253

255

View full text Add to dashboard Cite

“…Severe stress, such as burn injury, may also reduce the inflammatory responses to bacterial infections [34] . However, such stress is quite different from in vivo LPS tolerance since Kupffer cells/ macrophages after burn injury show a markedly reduced phagocytic activity and contribute to the aggravation of infectious diseases [11] .…”

Section: Cd68mentioning

confidence: 99%

In vivo Lipopolysaccharide Tolerance Recruits CD11b<sup>+</sup> Macrophages to the Liver with Enhanced Bactericidal Activity and Low Tumor Necrosis Factor-Releasing Capability, Resulting in Drastic Resistance to Lethal Septicemia

Kinoshita

Miyazaki²,

Nakashima³

et al. 2017

J Innate Immun

Self Cite

View full text Add to dashboard Cite

Objectives: In vivo lipopolysaccharide (LPS) tolerance on bacterial infection was investigated, focusing on liver macrophages. Methods: LPS tolerance was induced by intraperitoneal injections with 5 μg/kg of LPS for 3 consecutive days, and then mice were intravenously infected with Escherichia coli. Results: All LPS-primed mice survived lethal bacterial infection. Drastic enhancement of bactericidal activity of liver macrophages strongly contributed to bacterial clearance. Although LPS-primed mice produced substantial amounts of tumor necrosis factor (TNF) inside the liver, TNF efflux into the systemic circulation was markedly suppressed. These mice showed a dramatic increase in CD11b⁺ monocyte- derived macrophages in the liver. The CD11b⁺ macrophages that increased in LPS-primed mice were those with strong phagocytic/bactericidal activity and an upregulated expression of Fcγ receptor I, but the subfraction with a potent TNF-producing capacity and poor phagocytic activity diminished. The adoptive transfer of CD11b⁺ macrophages from LPS-primed mice to control mice increased survival after bacterial infection and reduced the elevation of plasma TNF. LPS priming did not affect the CD68⁺ resident Kupffer cells, and CD68⁺ Kupffer cell-depleted mice still exhibited LPS tolerance with strong resistance to bacteremia. Conclusions: LPS tolerance recruits CD11b⁺ macrophages to the liver with enhanced bactericidal activity, which plays a central role in resistance to lethal bacteremia.

show abstract

“…After neutrophils were stained with phycoerythrin (PE)-conjugated anti-mouse Gr-1 monoclonal antibody ([MAb] eBioscience, San Diego, CA), phagocytosis of FITC-microspheres by Gr-1 ϩ neutrophils was analyzed using an Epics XL flow cytometer (Beckman Coulter Inc., Miami, FL). FITC fluorescent intensity is dependent on the number of ingested microspheres (14). Peaks of the histogram correspond to neutrophils that contain no ingested microspheres or one (peak 1), two (peak 2), or more (peak Ն3) microspheres, as shown in Fig.…”

Section: Methodsmentioning

confidence: 99%

Enhancement of Neutrophil Function by Interleukin-18 Therapy Protects Burn-Injured Mice from Methicillin-Resistant Staphylococcus aureus

et al. 2011

Self Cite

View full text Add to dashboard Cite

Methicillin-resistantStaphylococcus aureus(MRSA) infection is a grave concern in burn-injured patients. We investigated the efficacy of interleukin-18 (IL-18) treatment in postburn MRSA infection. Alternate-day injections of IL-18 into burn-injured C57BL/6 mice significantly increased their survival after MRSA infection and after methicillin-sensitiveS. aureusinfection. Although IL-18 treatment of burn-injured mice augmented natural IgM production before MRSA infection and gamma interferon (IFN-γ) production after MRSA infection, neither IgM nor IFN-γ significantly contributed to the improvement in mouse survival. IL-18 treatment increased/restored the serum tumor necrosis factor (TNF), IL-17, IL-23, granulocyte colony-stimulating factor (G-CSF), and macrophage inflammatory protein (MIP-2) levels, as well as the neutrophil count, after MRSA infection of burn-injured mice; it also improved impaired neutrophil functions, phagocytic activity, production of reactive oxygen species, and MRSA-killing activity. However, IL-18 treatment was ineffective against MRSA infection in both burn- and sham-injured neutropenic mice. Enhancement of neutrophil functions by IL-18 was also observedin vitro. Furthermore, when neutrophils from IL-18-treated burn-injured mice were adoptively transferred into nontreated burn-injured mice 2 days after MRSA challenge, survival of the recipient mice increased. NOD-SCID mice that have functionally intact neutrophils and macrophages (but not T, B, or NK cells) were substantially resistant to MRSA infection. IL-18 treatment increased the survival of NOD-SCID mice after burn injury and MRSA infection. An adoptive transfer of neutrophils using NOD-SCID mice also showed a beneficial effect of IL-18-activated neutrophils, similar to that seen in C57BL/6 mice. Thus, although neutrophil functions were impaired in burn-injured mice, IL-18 therapy markedly activated neutrophil functions, thereby increasing survival from postburn MRSA infection.

show abstract

Novel mechanism of C‐reactive protein for enhancing mouse liver innate immunity†

Cited by 56 publications

References 33 publications

Characterization of two F4/80-positive Kupffer cell subsets by their function and phenotype in mice

Characterization of two F4/80-positive Kupffer cell subsets by their function and phenotype in mice

In vivo Lipopolysaccharide Tolerance Recruits CD11b<sup>+</sup> Macrophages to the Liver with Enhanced Bactericidal Activity and Low Tumor Necrosis Factor-Releasing Capability, Resulting in Drastic Resistance to Lethal Septicemia

Enhancement of Neutrophil Function by Interleukin-18 Therapy Protects Burn-Injured Mice from Methicillin-Resistant Staphylococcus aureus

Contact Info

Product

Resources

About