scholarly journals The anti-CD14 antibody IC14 suppresses ex vivo endotoxin stimulated tumor necrosis factor-alpha in patients with chronic heart failure

2006 ◽  
Vol 8 (4) ◽  
pp. 366-372 ◽  
Author(s):  
Sabine Genth-Zotz ◽  
Stephan von Haehling ◽  
Aidan P. Bolger ◽  
Paul R. Kalra ◽  
Roland Wensel ◽  
...  
2012 ◽  
Vol 93 (3) ◽  
pp. 494-498 ◽  
Author(s):  
A G Kuzmin ◽  
V V Gorbunov ◽  
E V Goryainova ◽  
E V Bogatikov ◽  
O D Koshevaya

Aim. To determine the changes in the content of cytokines, systolic intraventricular and interventricular dyssynchrony in patients with chronic heart failure. Methods. The study included 223 patients (174 males, 49 females) who suffered a Q wave myocardial infarction of the left ventricle, with clinical manifestations of chronic heart failure with functional class III according to the classification of the New York Heart Association. Pro- and anti-inflammatory cytokines (tumor necrosis factor alpha, interleukin-6, -4, and -10, interferon-gamma) were studied in blood plasma by enzyme immunoassay. Dyssynchrony was studied by pulsed-wave Doppler investigation, M-mode measurements of the left ventricle and pulsed-wave mode of tissue Doppler investigation of the myocardium. Results. Noted was an elevation of levels of tumor necrosis factor alpha, interleukin-6, interferon gamma, in combination with a reduction in the content of interleukin-4 and -10 in all groups. The maximum increase in the content of tumor necrosis factor alpha and interleukin-6 was found in the group of eccentric hypertrophy and dilatation of the left ventricle. Positive correleation links of medium strength have been established between the levels of interleukin-6 and the degree of interventricular mechanical delay, and between systolic and diastolic myocardial stress. In the group with eccentric hypertrophy and dilation of the left ventricle the content of tumor necrosis factor alpha directly correlated with the time interval from the beginning of the Q wave on the electrocardiogram to the beginning of the oflow in the left ventricular outflow tract, as well as with the concentration of N-terminal fragment of the precursor of the human brain natriuretic peptide. During remodeling according to the type of eccentric hypertrophy without dilatation of the left ventricle observed were positive correlation links of medium strength between the content of the tumor necrosis factor alpha and the intraventricular mechanical delay, end-diastolic pressure in the left ventricle. In the group of concentric hypertrophy the content of the tumor necrosis factor alpha and interleukin-6 is positively associated with electrocardiographic interval from the Q wave to the beginning of the systolic Doppler artifact S. Conclusion. One of the factors, which contributes to the preservation of abnormal levels of tumor necrosis factor alpha and interleukin-6 in blood plasma is the intraventricular and interventricular dyssynchrony; the combination of dilatation, myocardial hypertrophy, systolic and diastolic left ventricular dysfunction, dyssynchrony and the toxic effects of proinflammatory cytokines on the myocardium contributes to progression of chronic heart failure.


2000 ◽  
Vol 68 (9) ◽  
pp. 5234-5240 ◽  
Author(s):  
Catherine Newton ◽  
Shannon McHugh ◽  
Ray Widen ◽  
Noriya Nakachi ◽  
Thomas Klein ◽  
...  

ABSTRACT Infection of BALB/c mice with a sublethal concentration ofLegionella pneumophila causes an acute disease that is resolved by innate immune responses. The infection also initiates the development of adaptive Th1 responses that protect the mice from challenge infections. To study the early responses, cytokines induced during the first 24 h after infection were examined. In the serum, interleukin-12 (IL-12) was detectable by 3 h and peaked at 10 h, while gamma interferon was discernible by 5 h and peaked at 8 h. Similar patterns were observed in ex vivo cultures of splenocytes. A transient IL-4 response was also detected by 3 h postinfection in ex vivo cultures. BALB/c IL-4-deficient mice were more susceptible to L. pneumophila infection than were wild-type mice. The infection induced higher serum levels of acute-phase cytokines (tumor necrosis factor alpha [TNF-α], IL-1β, and IL-6), and reducing TNF-α levels with antibodies protected the mice from death. Moreover, the addition of IL-4 to L. pneumophila-infected macrophage cultures suppressed the production of these cytokines. Thus, the lack of IL-4 in the deficient mice resulted in unchecked TNF-α production, which appeared to cause the mortality. Monocyte chemoattractant protein-1 (MCP-1), a chemokine that is induced by IL-4 during Listeria monocytogenesinfection, was detected at between 2 and 30 h after infection. However, MCP-1 did not appear to be induced by IL-4 or to be required for the TNF-α regulation by IL-4. The data suggest that the early increase in IL-4 serves to regulate the mobilization of acute phase cytokines and thus controls the potential harmful effects of these cytokines.


1999 ◽  
Vol 5 (3) ◽  
pp. 61
Author(s):  
Yutaka Ishibashl ◽  
Takashi Sugamori ◽  
Nobuyuki Takahashi ◽  
Takeshi Sakane ◽  
Shuzo Ohhata ◽  
...  

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