Effect of Butonal-extracted Food Allergy Herbal Formula 2 (FAFH2) and its sub-fractions on TNF-alpha production by macrophage cells

We analyzed differences in host regulation of tumor necrosis factor-alpha (TNF-alpha) production and pathophysiological responses in conscious rats after infection with two strains of pathogenic Candida albicans spp. (CA-1 and CA-2) compared with Escherichia coli serotype 055:B5 (EC). The hypothesis was tested that, in contrast to EC, hypotension, organ injury, and mortality after candidemia are not obligatorily dependent on TNF-alpha or TNF-alpha-induced cyclooxygenase pathway metabolites. Dose, viability, and strain-specific dependencies were established after intravenous 10(6) or 10(9) viable CA, as well as heat-killed (HK) or Formalin-inactivated (FI) CA blastospores, compared with live EC at the 24-h LD25 [10(9) colony-forming units (CFU)] and LD100 (10(10) CFU). Shock without endotoxemia developed 4–8 h after 10(9) live CA-1 or CA-2 (LD100 at 24 h) with disseminated yeast-mycelial transformation and increased microvascular permeability in multiple organs but not after HK or FI CA-1. Peak serum TNF-alpha after an LD100 of CA-1 or CA-2 was < 3% of LD25 EC values and was < 1% of peak values during lethal bacteremia. Similar pathogen-specific differences were found in liver- and lung-associated TNF. Production of functionally inactive TNF-alpha during candidemia was excluded by enzyme-linked immunosorbent assay and sodium dodecyl sulfate-polyacrylamide gel electrophoresis with Western blotting. Passive immunization against TNF-alpha 2 h before microbial challenge was not protective against CA but prevented otherwise lethal EC sepsis. Cyclooxygenase inhibition also failed to attenuate candidemic shock. We conclude that the magnitude and kinetics of TNF-alpha production and TNF-alpha-dependent immunophysiological responses are differentially regulated after lethal fungal vs. gram-negative bacterial infection. Thus TNF-alpha is not a pivotal mediator of the acute Candida septic shock syndrome with disseminated candidiasis.

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The mechanisms of prednisone inhibition of inflammation in Crohn?s disease involve changes in intestinal permeability, mucosal TNF$alpha; production and nuclear factor kappa B expression

The American Journal of Gastroenterology ◽

10.1016/s0002-9270(01)03772-8 ◽

2001 ◽

Vol 96 (9) ◽

pp. S313

Author(s):

G WILD1

Keyword(s):

Intestinal Permeability ◽

Nuclear Factor Kappa B ◽

Tnf Alpha ◽

Nuclear Factor ◽

Nuclear Factor Kappa ◽

Alpha Production

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Efficacy, safety and immunological actions of butanol-extracted Food Allergy Herbal Formula-2 on peanut anaphylaxis

Clinical & Experimental Allergy ◽

10.1111/j.1365-2222.2010.03643.x ◽

2010 ◽

Vol 41 (4) ◽

pp. 582-591 ◽

Cited By ~ 19

Author(s):

K. Srivastava ◽

N. Yang ◽

Y. Chen ◽

I. Lopez-Exposito ◽

Y. Song ◽

...

Keyword(s):

Food Allergy ◽

Herbal Formula

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Elevated TNF-alpha production by peripheral blood monocytes of weight-losing COPD patients.

American Journal of Respiratory and Critical Care Medicine ◽

10.1164/ajrccm.153.2.8564110 ◽

1996 ◽

Vol 153 (2) ◽

pp. 633-637 ◽

Cited By ~ 198

Author(s):

I de Godoy ◽

M Donahoe ◽

W J Calhoun ◽

J Mancino ◽

R M Rogers

Keyword(s):

Peripheral Blood ◽

Tnf Alpha ◽

Blood Monocytes ◽

Peripheral Blood Monocytes ◽

Alpha Production ◽

Copd Patients

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The antagonist activity of lipid IVa on the stimulation by lipid A of TNF-alpha production from canine blood mononuclear cells

Veterinary Immunology and Immunopathology ◽

10.1016/j.vetimm.2011.06.024 ◽

2011 ◽

Vol 143 (1-2) ◽

pp. 167-169

Author(s):

Kenji Takasawa ◽

Rui Kano ◽

Haruhiko Maruyama ◽

Atsuhiko Hasegawa ◽

Hiroshi Kamata

Keyword(s):

Lipid A ◽

Mononuclear Cells ◽

Tnf Alpha ◽

Antagonist Activity ◽

Alpha Production ◽

Blood Mononuclear Cells

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Lipopolysaccharide-induced selective priming effects on tumor necrosis factor alpha and nitric oxide production in mouse peritoneal macrophages.

Journal of Experimental Medicine ◽

10.1084/jem.177.2.511 ◽

1993 ◽

Vol 177 (2) ◽

pp. 511-516 ◽

Cited By ~ 120

Author(s):

X Zhang ◽

D C Morrison

Keyword(s):

Tumor Necrosis ◽

Peritoneal Macrophages ◽

Tnf Alpha ◽

No Production ◽

Necrosis Factor Alpha ◽

Priming Effects ◽

Alpha Production ◽

Factor Alpha ◽

Mouse Peritoneal Macrophages ◽

Necrosis Factor

Preculture of thioglycollate-elicited C3HeB/FeJ mouse peritoneal macrophages in vitro with subthreshold stimulatory concentrations of lipopolysaccharide (LPS) can induce hyporesponsiveness (desensitization) to both tumor necrosis factor alpha (TNF-alpha) and nitric oxide (NO) production when these cells are subsequently stimulated with 100 ng/ml of LPS. We have established, however, that the primary dose of LPS required for inducing downregulation of NO production is significantly lower than that required for inducing downregulation of TNF-alpha production. Further, when LPS-pretreated macrophages become refractory to subsequent LPS stimulation for NO production, the secondary LPS-stimulated TNF-alpha production is markedly enhanced, and vice versa. These results indicate that LPS-induced TNF-alpha and NO production by macrophages are differentially regulated, and that the observed desensitization process may not reflect a state in which macrophages are totally refractory to subsequent LPS stimulation. Rather, our data suggest that LPS-pretreated macrophages become selectively primed for differential responses to LPS. The LPS-induced selective priming effects are not restricted to LPS stimulation, but extend as well to stimuli such as zymosan, Staphylococcus aureus, and heat-killed Listeria monocytogenes.

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