Role of C fibers in the inflammatory response to intratracheal lipopolysaccharide

1996 ◽  
Vol 271 (3) ◽  
pp. L425-L431 ◽  
Author(s):  
N. C. Long ◽  
C. W. Frevert ◽  
S. A. Shore
Keyword(s):  
Inflammatory Response ◽  
Alveolar Macrophages ◽  
Tumor Necrosis ◽  
Pulmonary Inflammation ◽  
Intratracheal Instillation ◽  
C Fibers ◽  
Vehicle Treatment ◽  
Necrosis Factor

We proposed that C fibers play a role in mediating the inflammatory response to the intratracheal instillation of lipopolysaccharaide (LPS), a purified form of endotoxin. To test this hypothesis, we compared the inflammatory response to intratracheal LPS (0.1-2.5 mg/kg) in rats whose C fibers had been destroyed by neonatal capsaicin treatment to the response seen in animals that were treated with vehicle. Three hours after the instillation of LPS, we assessed pulmonary inflammation by performing bronchoalveolar lavage (BAL) on the animals. We measured the number of neutrophils, the concentration of protein as an index of vascular permeability, and the concentration of tumor necrosis factor (TNF). Our results indicate that capsaicin treatment resulted in more neutrophils and higher levels of protein and TNF in the BAL fluid in response to intratracheal LPS, compared with vehicle treatment. Using cells from both groups of rats, we also assessed the production of inflammatory mediators by alveolar macrophages incubated with LPS (0.3-30 ng/ml) in vitro. We found a modest increase in the concentration of TNF and nitrite in the supernatant of macrophages collected from capsaicin-treated rats, in comparison with vehicle-treated animals. These results are consistent with the hypothesis that intrinsic differences in the sensitivity of alveolar macrophages of capsaicin and vehicle-treated animals contribute to the greater inflammatory response of capsaicin-treated rat to intratracheal LPS.

In Vitro Acute Effects of Tobacco Smoke on Tumor Necrosis Factor a and Interleukin-6 Production by Alveolar Macrophages

1993 ◽  
Vol 19 (3) ◽  
pp. 345-359 ◽  
Author(s):  
VÉRonique Dubar ◽  
Philippe Gosset ◽  
Colette Aerts ◽  
Cyr Voisin ◽  
Benoit Wallaert ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tobacco Smoke ◽  
Alveolar Macrophages ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Acute Effects ◽  
Necrosis Factor

scholarly journals Expression and functional role of tumor necrosis factor receptors on leukemic cells from patients with type B chronic lymphoproliferative disorders

Blood ◽  
1993 ◽  
Vol 81 (3) ◽  
pp. 752-758 ◽  
Author(s):  
L Trentin ◽  
R Zambello ◽  
C Agostini ◽  
F Siviero ◽  
F Adami ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Functional Role ◽  
Tumor Necrosis ◽  
Leukemic Cells ◽  
Tnf Alpha ◽  
High Affinity ◽  
Necrosis Factor

Abstract Two receptors for tumor necrosis factor (TNF) with different molecular weight (75-Kd and 55-Kd) and binding affinity have been recently discovered. To investigate the distribution and the functional role of these receptors on leukemic B cells from hairy cell leukemia (HCL) and B-cell chronic lymphocytic leukemia (B-CLL) patients, we evaluated: (1) the cytofluorimetric pattern of uncultured and cultured leukemic B cells incubated with utr-1 and htr-9 monoclonal antibodies (MoAbs), which specifically recognize the 75-Kd and 55-Kd TNF receptors (TNFR), respectively; (2) the effect of TNF-alpha and TNF-beta on leukemic B cells in an in vitro proliferation assay; (3) the role of anti-TNFR MoAbs on TNF-alpha and TNF-beta-driven B-cell growth; and (4) the proliferative effect of utr-1 and htr-9 MoAbs on in vitro cultured leukemic cells. Our study shows that the high affinity (75-Kd) but not the low affinity (55-Kd) TNFR molecules are expressed on freshly isolated leukemic B cells recovered from HCL and B-CLL patients. The expression of these receptors was neither upregulated nor downregulated by different stimuli, including TNF-alpha, TNF-beta, B-cell growth factor, and interleukin-2. TNF-alpha efficiently triggers the proliferation of HC and, to a lesser extent, the growth of B-CLL cells. TNF-beta was also able to transduce the proliferative signal in HCL, but not in B-CLL patients. TNF-alpha- and TNF-beta-driven B-cell proliferation was inhibited by the preincubation of leukemic B cells with utr-1 but not htr-9 MoAb. Moreover, anti-75-Kd, but not anti-55-Kd TNFR MoAb, was able to trigger the proliferation of leukemic B cells, and in particular of HC. These results show that leukemic B cells from patients with HCL and B-CLL are equipped with a fully functional high affinity TNFR.

Tumor necrosis factor α plus interleukin 1β treatment protects granulocytopenic mice fromPseudomonas aeruginosalung infection: Role of an unusual inflammatory response

Apmis ◽  
1995 ◽  
Vol 103 (1-6) ◽  
pp. 447-459 ◽  
Author(s):  
CLAUDIA R. Amura ◽  
PATRICIA A. Fontan ◽  
NORBERTO Sanjuan ◽  
MARCELO M. Nociari ◽  
FERNANDA R. Buzzola ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Inflammatory Response ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Interleukin 1Β ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Krüppel-Like Factor 4 Is a Regulator of Proinflammatory Signaling in Fibroblast-Like Synoviocytes through Increased IL-6 Expression

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Xinjing Luo ◽  
Jie Chen ◽  
Jianwei Ruan ◽  
Yongfeng Chen ◽  
Xuanrong Mo ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Vital Role ◽  
Cytokine Tumor Necrosis Factor ◽  
Synovial Tissues ◽  
Necrosis Factor ◽  
Fibroblast Like Synoviocytes

Human fibroblast-like synoviocytes play a vital role in joint synovial inflammation in rheumatoid arthritis (RA). Proinflammatory cytokines induce fibroblast-like synoviocyte activation and dysfunction. The inflammatory mediator Krüppel-like factor 4 is upregulated during inflammation and plays an important role in endothelial and macrophage activation during inflammation. However, the role of Krüppel-like factor 4 in fibroblast-like synoviocyte activation and RA inflammation remains to be defined. In this study, we identify the notion that Krüppel-like factor 4 is higher expressed in synovial tissues and fibroblast-like synoviocytes from RA patients than those from osteoarthritis patients.In vitro, the expression of Krüppel-like factor 4 in RA fibroblast-like synoviocytes is induced by proinflammatory cytokine tumor necrosis factor-α. Overexpression of Krüppel-like factor 4 in RA fibroblast-like synoviocytes robustly induced interleukin-6 production in the presence or absence of tumor necrosis factor-α. Conversely, knockdown of Krüppel-like factor 4 markedly attenuated interleukin-6 production in the presence or absence of tumor necrosis factor-α. Krüppel-like factor 4 not only can bind to and activate the interleukin-6 promoter, but also may interact directly with nuclear factor-kappa B. These results suggest that Krüppel-like factor 4 may act as a transcription factor mediating the activation of fibroblast-like synoviocytes in RA by inducing interleukin-6 expression in response to tumor necrosis factor-α.

Sign in / Sign up

Export Citation Format

Share Document