scholarly journals Dynamics of cytokine activity of cerebrospinal fluid and blood serum of carnivores with pain syndrome

2021 ◽  
pp. 52-55
Author(s):  
Sergey Dmitrievich Klyukin ◽  
Vladimir Vasilyevich Salautin ◽  
Sergey Vasilyevich Kozlov ◽  
Nikolai Alexandrovich Pudovkin ◽  
Daniil Sergeevich Frolov

New data on the mechanisms of pain syndrome development in dogs and cats were obtained, in particular, the role of anti - inflammatory cytokines: interleukin-4 (IL-4), interleukin-6 (IL - 6), interferon - gamma (IFN - gamma), tumor necrosis factor - alpha (TNF-alfa) in the formation and manifestation of this pathology was determined. The results obtained allow us to assess the dynamics of the immune status of animals with pain syndrome. Cytokines: IL-4, IL-6, and IFN - gamma showed high significance in the diagnosis of pain syndrome. Thus, the values of IL-4 in the cerebrospinal fluid and blood serum in dogs in the first experimental group were 3.5 times and 3.4 times higher in the second experimental group than in the control, in cats of the first experimental group-4.3 and 4.6 times in the second experimental group. As well as IL-4, both IL - 6 and IFN - gamma showed their high activity, in contrast to TNF-alfa, which was less sensitive to changes in pain syndrome.

2004 ◽  
Vol 72 (7) ◽  
pp. 3932-3940 ◽  
Author(s):  
Celina Arruda ◽  
Rita C. Valente-Ferreira ◽  
Adriana Pina ◽  
Suely S. Kashino ◽  
Raquel A. Fazioli ◽  
...  

ABSTRACT Resistance to paracoccidioidomycosis, the most important endemic mycosis in Latin America, is thought to be primarily mediated by cellular immunity and the production of gamma interferon. To assess the role of interleukin-4 (IL-4), a Th2 cytokine, pulmonary paracoccidioidomycosis in IL-4-depleted susceptible (B10.A) and intermediate (C57BL/6) mice was studied. Two different protocols were used to neutralize endogenous IL-4 in B10.A mice: 1 mg of anti-IL-4 monoclonal antibody (MAb)/week and 8 mg 1 day before intratracheal infection with 106 Paracoccidioides brasiliensis yeast cells. Unexpectedly, both protocols enhanced pulmonary infection but did not alter the levels of pulmonary cytokines and specific antibodies. Since in a previous work it was verified that C57BL/6 mice genetically deficient in IL-4 were more resistant to P. brasiliensis infection, we also investigated the effect of IL-4 depletion in this mouse strain. Treatment with the MAb at 1 mg/week led to less severe pulmonary disease associated with impaired synthesis of Th2 cytokines in the lungs and liver of control C57BL/6 mice. Conversely, in IL-4-depleted C57BL/6 mice, increased levels of tumor necrosis factor alpha and IL-12 were found in the lungs and liver, respectively. In addition, higher levels of immunoglobulin G2a (IgG2a) and lower levels of IgG1 antibodies were produced by IL-4-depleted mice than by control mice. Lung pathologic findings were equivalent in IL-4-depleted and untreated B10.A mice. In IL-4-depleted C57BL/6 mice, however, smaller and well-organized granulomas replaced the more extensive lesions that developed in untreated mice. These results clearly showed that IL-4 can have a protective or a disease-promoting effect in pulmonary paracoccidioidomycosis depending on the genetic background of the host.


Blood ◽  
1990 ◽  
Vol 76 (7) ◽  
pp. 1392-1397 ◽  
Author(s):  
AA te Velde ◽  
RJ Huijbens ◽  
K Heije ◽  
JE de Vries ◽  
CG Figdor

Monocytes activated by lipopolysaccharide (LPS) and interferon gamma (IFN gamma) rapidly secrete a number of monokines with different functional properties. Interleukin–4 (IL–4), a T-cell derived cytokine, has been shown to reduce the production of monokines with cytostatic activity for tumor cells, chemotactic activity for monocytes, and factors that stimulate thymocyte proliferation. This latter activity is mediated by a number of monokines like IL–1, tumor necrosis factor alpha (TNF alpha), and IL–6. To elucidate which cytokines produced by monocytes are controlled by IL–4, we tested the effect of IL–4 on the secretion of IL–1 alpha, IL–1 beta, TNF alpha, and IL–6 induced by LPS or IFN gamma. IL–4 was found to inhibit the secretion of IL–1 beta and TNF alpha by activated monocytes almost 100%. The secretion of IL–6 was found to be reduced 70% to 85% in the presence of IL–4, whereas there was no effect on the secretion of IL–1 alpha (IL–1 alpha is mainly cell- associated). Time-course experiments demonstrate that IL–4 reduces the secretion of monokines for a prolonged period of time (greater than 40 hours). The reduced secretion of IL–1 beta and TNF alpha was specifically induced by IL–4 because anti-IL–4 antiserum completely restored normal monokine production. These data suggest that IL–4 plays a role in the regulation of immune responses by reducing the production of functionally important monokines.


Blood ◽  
1990 ◽  
Vol 76 (7) ◽  
pp. 1392-1397 ◽  
Author(s):  
AA te Velde ◽  
RJ Huijbens ◽  
K Heije ◽  
JE de Vries ◽  
CG Figdor

Abstract Monocytes activated by lipopolysaccharide (LPS) and interferon gamma (IFN gamma) rapidly secrete a number of monokines with different functional properties. Interleukin–4 (IL–4), a T-cell derived cytokine, has been shown to reduce the production of monokines with cytostatic activity for tumor cells, chemotactic activity for monocytes, and factors that stimulate thymocyte proliferation. This latter activity is mediated by a number of monokines like IL–1, tumor necrosis factor alpha (TNF alpha), and IL–6. To elucidate which cytokines produced by monocytes are controlled by IL–4, we tested the effect of IL–4 on the secretion of IL–1 alpha, IL–1 beta, TNF alpha, and IL–6 induced by LPS or IFN gamma. IL–4 was found to inhibit the secretion of IL–1 beta and TNF alpha by activated monocytes almost 100%. The secretion of IL–6 was found to be reduced 70% to 85% in the presence of IL–4, whereas there was no effect on the secretion of IL–1 alpha (IL–1 alpha is mainly cell- associated). Time-course experiments demonstrate that IL–4 reduces the secretion of monokines for a prolonged period of time (greater than 40 hours). The reduced secretion of IL–1 beta and TNF alpha was specifically induced by IL–4 because anti-IL–4 antiserum completely restored normal monokine production. These data suggest that IL–4 plays a role in the regulation of immune responses by reducing the production of functionally important monokines.


1999 ◽  
Vol 67 (9) ◽  
pp. 4921-4925 ◽  
Author(s):  
Ingela Ahlstedt ◽  
Catharina Lindholm ◽  
Hans Lönroth ◽  
Annika Hamlet ◽  
Ann-Mari Svennerholm ◽  
...  

ABSTRACT Using immunohistochemical staining, we examined the presence of secretory component (SC) on epithelial cells in gastric and duodenal biopsy specimens collected from Helicobacter pylori-infected individuals and healthy controls. Gastric epithelial cells from healthy volunteers expressed low, but detectable, levels of SC. In contrast, significantly higher level of expression of SC (P < 0.001) was observed on epithelial cells in the antra of H. pylori-infected individuals. The antral SC expression correlated with staining for gamma interferon of intraepithelial and lamina propria lymphocytes (r s = 0.76 and 0.69, respectively,P < 0.001) and correlated weakly with production of tumor necrosis factor alpha (r s = 0.43,P < 0.05), but it did not correlate at all with interleukin-4 production.


2009 ◽  
Vol 8 (2) ◽  
pp. 67-71 ◽  
Author(s):  
O. Ye. Chechina ◽  
A. K. Biktasova ◽  
Ye. V. Sazonova ◽  
O. B. Zhukova ◽  
T. S. Prokhorenko ◽  
...  

Research of influence of recombinant tumor necrosis factor alpha, interleukin-2 and interleukin-4 in vitro on the apoptosis of lymphocytes is performed. It is revealed that a proapoptotic effect of these cytokines is dose-dependent and is realized with the assistance of reactive oxygen species and mitochondrias.


2004 ◽  
Vol 72 (8) ◽  
pp. 4552-4560 ◽  
Author(s):  
Miriam Rodríguez-Sosa ◽  
Rafael Saavedra ◽  
Eda P. Tenorio ◽  
Lucia E. Rosas ◽  
Abhay R. Satoskar ◽  
...  

ABSTRACT To determine the role of STAT4-dependent Th1 responses in the regulation of immunity to the helminth parasite Taenia crassiceps, we monitored infections with this parasite in resistant mice lacking the STAT4 gene. While T. crassiceps-infected STAT4+/+ mice rapidly resolved the infection, STAT4−/− mice were highly susceptible to infection and displayed large parasite loads. Moreover, the inability of STAT4−/− mice to control the infection was associated with the induction of an antigen-specific Th2-type response characterized by significantly higher levels of Th2-associated immunoglobulin G1 (IgG1) and total IgE as well as interleukin-4 (IL-4), IL-10, and IL-13 than those in STAT4+/+ mice, who produced significantly more gamma interferon. Furthermore, early after infection, macrophages from STAT4−/− mice produced lower levels of the pro-inflammatory cytokines IL-12, tumor necrosis factor alpha, IL-1β, and nitric oxide (NO) than those from STAT4+/+ mice, suggesting a pivotal role for macrophages in mediating protection against cysticercosis. These findings demonstrate a critical role for the STAT4 signaling pathway in the development of a Th1-type immune response that is essential for mediating protection against the larval stage of T. crassiceps infection.


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