scholarly journals Roles of Interleukin‐6 and Macrophage Inflammatory Protein–2 in Pneumolysin‐Induced Lung Inflammation in Mice

2002 ◽  
Vol 185 (1) ◽  
pp. 123-126 ◽  
Author(s):  
Anita W. Rijneveld ◽  
Germie P. van den Dobbelsteen ◽  
Sandrine Florquin ◽  
Theodore J. Standiford ◽  
Peter Speelman ◽  
...  
Keyword(s):  
Interleukin 6 ◽  
Lung Inflammation ◽  
Inflammatory Protein ◽  
Macrophage Inflammatory Protein

Fever induced by macrophage inflammatory protein-1β in the rat is independent of hypothalamic interleukin-1β or interleukin-6

2000 ◽  
Vol 25 (1-2) ◽  
pp. 5-10 ◽  
Author(s):  
Khalid Benamar ◽  
Antonio Fernández-Alonso ◽  
Eva Tavares ◽  
Francisco J López-Valpuesta ◽  
Manuel Sancibrián ◽  
...  
Keyword(s):  
Interleukin 6 ◽  
Interleukin 1Β ◽  
Inflammatory Protein ◽  
Macrophage Inflammatory Protein

Associations of interleukin-6 with interleukin-1β, interleukin-8 and macrophage inflammatory protein-1β in midlife women

Cytokine ◽  
2008 ◽  
Vol 41 (3) ◽  
pp. 302-306 ◽  
Author(s):  
Toshiyuki Yasui ◽  
Hirokazu Uemura ◽  
Masayo Yamada ◽  
Toshiya Matsuzaki ◽  
Naoko Tsuchiya ◽  
...  
Keyword(s):  
Interleukin 6 ◽  
Midlife Women ◽  
Interleukin 8 ◽  
Interleukin 1Β ◽  
Inflammatory Protein ◽  
Macrophage Inflammatory Protein

scholarly journals Effects of Exogenous Interleukin-6 duringPseudomonas aeruginosa Corneal Infection

2001 ◽  
Vol 69 (6) ◽  
pp. 4116-4119 ◽  
Author(s):  
Nerida Cole ◽  
Mark Krockenberger ◽  
Shisan Bao ◽  
Kenneth W. Beagley ◽  
Alan J. Husband ◽  
...  
Keyword(s):  
Interleukin 6 ◽  
Gene Knockout ◽  
Severe Disease ◽  
Neutrophil Recruitment ◽  
Wild Type ◽  
Corneal Infection ◽  
Inflammatory Protein ◽  
Cell Adhesion Molecule 1 ◽  
Intercellular Cell Adhesion Molecule ◽  
Macrophage Inflammatory Protein

ABSTRACT Lack of interleukin-6 (IL-6) during Pseudomonas aeruginosa corneal infection leads to more severe disease with changes in neutrophil recruitment. Exogenous IL-6 leads to increased efficiency of neutrophil recruitment and reduced bacterial loads in corneal infection in both IL-6 gene knockout and wild-type mice. This may be mediated by IL-6 increasing the production of corneal macrophage inflammatory protein 2 and intercellular cell adhesion molecule 1. We conclude that effective recruitment of neutrophils into the cornea is dependent on the production of IL-6 and that early augmentation of IL-6 may be protective in corneal infection.

scholarly journals Impaired Pulmonary NF-κB Activation in Response to Lipopolysaccharide in NADPH Oxidase-Deficient Mice

2001 ◽  
Vol 69 (10) ◽  
pp. 5991-5996 ◽  
Author(s):  
M. Audrey Koay ◽  
John W. Christman ◽  
Brahm H. Segal ◽  
Annapurna Venkatakrishnan ◽  
Thomas R. Blackwell ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Intracellular Signaling ◽  
Lung Inflammation ◽  
Nuclear Translocation ◽  
Binding Activity ◽  
Wild Type ◽  
Inflammatory Protein ◽  
Macrophage Inflammatory Protein ◽  
Deficient Mice

ABSTRACT Reactive oxygen species (ROS) are thought to be involved in intracellular signaling, including activation of the transcription factor NF-κB. We investigated the role of NADPH oxidase in the NF-κB activation pathway by utilizing knockout mice (p47phox−/−) lacking the p47phox component of NADPH oxidase. Wild-type (WT) controls and p47phox−/−mice were treated with intraperitoneal (i.p.) Escherichia coli lipopolysaccharide (LPS) (5 or 20 μg/g of body weight). LPS-induced NF-κB binding activity and accumulation of RelA in nuclear protein extracts of lung tissue were markedly increased in WT compared to p47phox−/− mice 90 min after treatment with 20 but not 5 μg of i.p. LPS per g. In another model of lung inflammation, RelA nuclear translocation was reduced in p47phox−/− mice compared to WT mice following treatment with aerosolized LPS. In contrast to NF-κB activation in p47phox−/− mice, LPS-induced production of macrophage inflammatory protein 2 in the lungs and neutrophilic lung inflammation were not diminished in these mice compared to WT mice. We conclude that LPS-induced NF-κB activation is deficient in the lungs of p47phox−/− mice compared to WT mice, but this abnormality does not result in overt alteration in the acute inflammatory response.

scholarly journals Vinpocetine alleviates lung inflammation via macrophage inflammatory protein-1β inhibition in an ovalbumin-induced allergic asthma model

PLoS ONE ◽  
2021 ◽  
Vol 16 (4) ◽  
pp. e0251012
Author(s):  
Won Seok Choi ◽  
Hyun Sik Kang ◽  
Hong Jo Kim ◽  
Wang Tae Lee ◽  
Uy Dong Sohn ◽  
...  
Keyword(s):  
Lung Inflammation ◽  
Allergic Inflammation ◽  
Inflammatory Cells ◽  
Specific Ige ◽  
Control Group ◽  
Bronchial Disease ◽  
Inflammatory Protein ◽  
Bronchial Inflammation ◽  
Bronchial Mucus ◽  
Macrophage Inflammatory Protein

Asthma is a well-known bronchial disease that causes bronchial inflammation, narrowing of the bronchial tubes, and bronchial mucus secretion, leading to bronchial blockade. In this study, we investigated the association between phosphodiesterase (PDE), specifically PDE1, and asthma using 3-isobutyl-1-methylxanthine (IBMX; a non-specific PDE inhibitor) and vinpocetine (Vinp; a PDE1 inhibitor). Balb/c mice were randomized to five treatment groups: control, ovalbumin (OVA), OVA + IBMX, OVA + Vinp, and OVA + dexamethasone (Dex). All mice were sensitized and challenged with OVA, except for the control group. IBMX, Vinp, or Dex was intraperitoneally administered 1 h before the challenge. Vinp treatment significantly inhibited the increase in airway hyper-responsiveness (P<0.001) and reduced the number of inflammatory cells, particularly eosinophils, in the lungs (P<0.01). It also ameliorated the damage to the bronchi and alveoli and decreased the OVA-specific IgE levels in serum, an indicator of allergic inflammation increased by OVA (P<0.05). Furthermore, the increase in interleukin-13, a known Th2 cytokine, was significantly decreased by Vinp (P<0.05), and Vinp regulated the release and mRNA expression of macrophage inflammatory protein-1β (MIP-1β) increased by OVA (P<0.05). Taken together, these results suggest that PDE1 is associated with allergic lung inflammation induced by OVA. Thus, PDE1 inhibitors can be a promising therapeutic target for the treatment of asthma.

Candida Soluble Cell Wall β-D-Glucan Induces Lung Inflammation in Mice

2007 ◽  
Vol 20 (3) ◽  
pp. 499-508 ◽  
Author(s):  
K. Inoue ◽  
H. Takano ◽  
T. Oda ◽  
R. Yanagisawa ◽  
H. Tamura ◽  
...  
Keyword(s):  
Cell Wall ◽  
Proinflammatory Cytokines ◽  
Lung Inflammation ◽  
Soluble Cell ◽  
Inflammatory Protein ◽  
Enhanced Expression ◽  
Factor Α ◽  
Macrophage Inflammatory Protein ◽  
Necrosis Factor

Bioactivity of cell wall component(s) of fungi has not been fully elucidated, especially in vivo. We isolated Candida soluble beta-D-glucan (CSBG) from Candida albicans (C. albicans). We investigated the effects of airway exposure to CSBG on the immune systems in the airways in mice. CSBG exposure induced neutrophilic and eosinophilic inflammation in the lung, which was concomitant with the increased local expression of proinflammatory cytokines including tumor necrosis factor - α, interleukin (IL)-1 β, IL-6, macrophage inflammatory protein -1 α, macrophage chemoattractant protein -1, RANTES (regulated on activation and normal T cells expressed and secreted), and eotaxin. The lung inflammation with enhanced expression of proinflammatory proteins caused by CSBG was directly related to its structure, since structurally degraded products of CSBG by formic acid induced negligible responses in the lung. CSBG enhanced nuclear localization of phosphorylated signal transducer and activator of transcription (STAT)-6 in the lung. These results suggest that airway exposure to CSBG induces lung inflammation, at least partly, via the enhanced expression of proinflammatory cytokines and the activation of STAT-6 pathway, and can be a proper murine model for fungal lung inflammation.

Fever and feeding in the rat: Actions of intrahypothalamic interleukin-6 compared to macrophage inflammatory protein-1β (MIP-1β)

1994 ◽  
Vol 39 (1) ◽  
pp. 31-37 ◽  
Author(s):  
R. D. Myers ◽  
F. J. Lopez-Valpuesta ◽  
F. J. Minñano ◽  
M. H. Wooten ◽  
V. S. Barwick ◽  
...  
Keyword(s):  
Interleukin 6 ◽  
Inflammatory Protein ◽  
Macrophage Inflammatory Protein

scholarly journals Hemorrhage Decreases Macrophage Inflammatory Protein 2 and Interleukin-6 Release

1999 ◽  
Vol 229 (5) ◽  
pp. 651 ◽  
Author(s):  
Martin K. Angele ◽  
Markus W. Knöferl ◽  
Martin G. Schwacha ◽  
Alfred Ayala ◽  
Kirby I. Bland ◽  
...  
Keyword(s):  
Interleukin 6 ◽  
Inflammatory Protein ◽  
Macrophage Inflammatory Protein

Role of the type 1 TNF receptor in lung inflammation after inhalation of endotoxin orPseudomonas aeruginosa

1999 ◽  
Vol 276 (5) ◽  
pp. L715-L727 ◽  
Author(s):  
Shawn J. Skerrett ◽  
Thomas R. Martin ◽  
Emil Y. Chi ◽  
Jacques J. Peschon ◽  
Kendall M. Mohler ◽  
...  
Keyword(s):  
Lung Inflammation ◽  
Interleukin 1Β ◽  
Intercellular Adhesion Molecule ◽  
Bacterial Clearance ◽  
Tnf Receptor ◽  
Protein Levels ◽  
Inflammatory Protein ◽  
Tnf Α ◽  
Macrophage Inflammatory Protein

To determine the roles of the type 1 tumor necrosis factor (TNF) receptor (TNFR1) in lung inflammation and antibacterial defense, we exposed transgenic mice lacking TNFR1 [TNFR1(−/−)] and wild-type control mice to aerosolized lipopolysaccharide or Pseudomonas aeruginosa. After LPS, bronchoalveolar lavage fluid (BALF) from TNFR1(−/−) mice contained fewer neutrophils and less macrophage inflammatory protein-2 than BALF from control mice. TNF-α, interleukin-1β, and total protein levels in BALF as well as tissue intercellular adhesion molecule-1 expression did not differ between the two groups. In contrast, lung inflammation and bacterial clearance after infection were augmented in TNFR1(−/−) mice. BALF from infected TNFR1(−/−) mice contained more neutrophils and TNF-α and less interleukin-1β and macrophage inflammatory protein-2 than that from control mice, but protein levels were similarly elevated in both groups. Lung inflammation and bacterial clearance were also augmented in mice lacking both TNF receptors. Thus TNFR1 facilitates neutrophil recruitment after inhalation of lipopolysaccharide, in part by augmenting chemokine induction. In contrast, TNFR1 attenuates lung inflammation in response to live bacteria but does not contribute to increased lung permeability and is not required for the elimination of P. aeruginosa.

Role of interleukin-1β, interleukin-6 and macrophage inflammatory protein-1β in prostaglandin-E2-induced hyperthermia in rats

Life Sciences ◽  
1996 ◽  
Vol 59 (12) ◽  
pp. PL185-PL190 ◽  
Author(s):  
A. Fernández-Alonso ◽  
K. Benamar ◽  
M. SancibriÁn ◽  
F.J. López-Valpuesta ◽  
F.J. Mifiano
Keyword(s):  
Prostaglandin E2 ◽  
Interleukin 6 ◽  
Interleukin 1Β ◽  
Induced Hyperthermia ◽  
Inflammatory Protein ◽  
Macrophage Inflammatory Protein
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