Interleukin-1 Beta (IL-1β) in the Peripheral Blood of Dogs as a Possible Marker for the Detection of Early Stages of Inflammation

Abstract

Background: Cytokines are mediators of disease. Expression levels in the blood could be of clinical relevance. Objective: Aim of this study was to show if serum levels of IL-1β could be of any clinical relevance concerning dogs. IL-1β was measured in serum samples of healthy dogs to find a reference range for healthy individuals. Measurements of IL-1β should show if this substance was a possible marker for early stages of inflammation. Therefore, a possible relation between serum levels and grades of leukocytosis was analyzed. Methods: IL-1β concentrations in the blood were assessed by the use of a human enzyme linked immunosorbent assay (ELISA). 39 dogs with different inflammatory diseases were analyzed to figure out if there was a correlation between IL-1β serum levels and the number of leukocytes in peripheral blood. The control group consisted of 16 healthy dogs. Results: about half of the samples IL-1β were detected. Most of the patients showed no detectable amounts of IL-1β. The IL-1β levels measured in the serum were stable for at least nine weeks when stored at ?20?C. The patients tested positively on IL-1β had mostly lower-grade leukocytosis compared to those who had no IL-1β in serum. All the dogs which were suffering from disease but still had no traceable IL-1β, showed a leukocytosis as a common symptom. Conclusion: This study showed that IL-1β could become an interesting marker for the detection of early stages of inflammation when leukocytosis does not yet appear in peripheral blood. Nonetheless, the possible use in diagnosis is restricted. This is due to the fact that there are only low amounts of IL-1β to be detected in the serum, even concerning patients are suffering from disease.

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C. Prachar, F. Kaup and S. Neumann, "Interleukin-1 Beta (IL-1β) in the Peripheral Blood of Dogs as a Possible Marker for the Detection of Early Stages of Inflammation," Open Journal of Veterinary Medicine, Vol. 3 No. 7, 2013, pp. 302-308. doi: 10.4236/ojvm.2013.37049.

Conflicts of Interest

The authors declare no conflicts of interest.

References

[1] C. A. Dinarello, “Biologic Basis for Interleukin-1 in Disease,” Blood, Vol. 87, No. 6, 1996, pp. 2095-2147.
[2] J. L. Telford, G. Macchia, A. Massone, V. Carinci, E. Palla and M. Melli, “The Murine Interleukin 1 Beta Gene: Structure and Evolution,” Nucleic Acids Research, Vol. 14, No. 24, 1986, pp. 9955-9963.
http://dx.doi.org/10.1093/nar/14.24.9955
[3] P. L. Kilian, K. L. Kaffka, A. S. Stern, D. Woehle, W. R. Benjamin, T. M. Dechiara, U. Gubler, J. J. Farrar, S. B. Mizel and P. T. Lomedico, “Interleukin 1 Alpha and Interleukin 1 Beta Bind to the Same Receptor on T Cells,” The Journal of Immunology, Vol. 136, No. 12, 1986, pp. 4509-4514.
[4] C. A. Meyers, K. O. Johanson, L. M. Miles, P. J. McDevitt, P. L. Simon, R. L. Webb, M. J. Chen, B. P. Holskin, J. S. Lillquist and P. R. Young, “Purification and Characterization of Human Recombinant Interleukin-1 Beta,” The Journal of Biological Chemistry, Vol. 262, No. 23, 1987, pp. 11176-11181.
[5] S. K. Durum, J. A. Schmidt and J. J. Oppenheim, “Interleukin 1: An Immunological Perspective,” Annual Review of Immunology, Vol. 3, No. 1, 1985, pp. 263-287.
http://dx.doi.org/10.1146/annurev.iy.03.040185.001403
[6] C. A. Dinarello, “Interleukin-1 and the Pathogenesis of the Acute-Phase Response,” The New England Journal of Medicine, Vol. 311, No. 22, 1984, pp. 1413-1418.
http://dx.doi.org/10.1056/NEJM198411293112205
[7] F. Ceciliani, A. Giordano and V. Spagnolo, “The Systemic Reaction during Inflammation: The Acute-Phase Proteins,” Protein and Peptide Letters, Vol. 9, No. 3, 2002, pp. 211-223.
http://dx.doi.org/10.2174/0929866023408779
[8] A Grone, S. Fonfara and W. Baumgartner, “Cell TypeDependent Cytokine Expression after Canine Distemper Virus Infectio,” Viral Immunology, Vol. 15, No. 3, 2002, pp. 493-505.
http://dx.doi.org/10.1089/088282402760312368
[9] M. F. Rai, P. S. Rachakondaa, K. Manning, B. Vorwerk, L. Brunnberg, B. Kohn, M. F. G. Schmidt, “Quantification of Cytokines and Inflammatory Mediators in a ThreeDimensional Model of Inflammatory Arthritis,” Cytokine, Vol. 42, No. 1, 2008, pp. 8-17.
http://dx.doi.org/10.1016/j.cyto.2008.02.004
[10] J. Y. Yhee, C.-H. Yu, J.-H. Kim and J.-H. Sur1, “Effects of T Lymphocytes, Interleukin-1, and Interleukin-6 on Renal Fibrosis in Canine End-Stage Renal Disease,” Journal of Veterinary Diagnostic Investigation, Vol. 20, No. 5, 2008, pp. 585-592.
http://dx.doi.org/10.1177/104063870802000508
[11] K. K. Al’tsivanovich and V. N. Gurin, “Activity of Blood Interleukin-1 in Dogs during Work Hyperthermia,” Bulletin of Experimental Biology and Medicine, Vol. 110, No. 12, 1990, pp. 565-567.
[12] J. T. Soller, H. Murua-Escobar, S. Willenbrock, M. Janssen, N. Eberle, J. Bullerdiek and I. Nolte, “Comparison of the Human and Canine Cytokines IL-1 (Alpha/Beta) and TNF-Alpha to Orthologous Other Mammalians,” Journal of Heredity, Vol. 98, No. 5, 2007, pp. 485-490.
http://dx.doi.org/10.1093/jhered/esm025
[13] T. Miyamoto, T. Fujinaga, K. Yamashita and M. Hagio, “Changes of Serum Cytokine Activities and Other Parameters in Dogs with Experimentally Induced Endotoxic Shock,” The Japanese Journal of Veterinary Research, Vol. 44, No. 2, 1996, pp. 107-118.
[14] V. Barak, C. Selmi, M. Schlesinger, M. Blank, N. Agmon-Levin, I. Kalickman, M. E. Gershwin and Y. Shoenfeld, “Serum Inflammatory Cytokines, Complement Components, and Soluble Interleukin 2 Receptor in Primary Biliary Cirrhosis,” Journal of Autoimmunity, Vol. 33, No. 3-4, 2009, pp. 178-182.
http://dx.doi.org/10.1016/j.jaut.2009.09.010
[15] E. A. Fernandez-Figueroa, et al., “Disease Severity in Patients Infected with Leishmania Mexicana Relates to IL-1β,” PLOS Neglected Tropical Diseases, Vol. 6, No. 5, 2012, p. E1533.
[16] B. Brugos, Z. Vincze, S. Sipka, G. Szegedi and M. Zeher, “Serum and Urinary Cytokine Levels of SLE Patients,” Pharmazie, Vol. 67, No. 5, 2012, pp. 411-413.
[17] S. Papin, S. Cuenin1, L. Agostini1, F. Martinon1, S. Werner, H.-D. Beer, C. Grütter, M. Grütter and J. Tschopp, “The SPRY Domain of Pyrin, Mutated in Familial Mediterranean Fever Patients, Interacts with Inflammasome Components and Inhibits Proil-1β Processing,” Cell Death and Differentiation, Vol. 14, No. 8, 2007, pp. 1457-1466. http://dx.doi.org/10.1038/sj.cdd.4402142
[18] S. M. Allan, P. J. Tyrrell and N. J. Rothwell, “Interleukin-1 and Neuronal Injury,” Nature Reviews Immunology, Vol. 5, No. 8, 2005, pp. 629-640.
http://dx.doi.org/10.1038/nri1664
[19] M. Kusuhara, K. Isoda and F. Ohsuzu, “Interleukin-1 and Occlusive Arterial Diseases,” Cardiovascular & Hematological Agents in Medicinal Chemistry, Vol. 4, No. 3, 2006, pp. 229-235.
http://dx.doi.org/10.2174/187152506777698335
[20] K. S. Kornman, “Interleukin 1 Genetics, Inflammatory Mechanisms, and Nutrigenetic Opportunities to Modulate Diseases of Aging,” The American Journal of Clinical Nutrition, Vol. 83, No. 2, 2006, pp. S475-S483.
[21] C. A. Dinarello, A. Simon and J. W. van der Meer, “Treating Inflammation by Blocking Interleukin-1 in a Broad Spectrum of Diseases,” Nature Reviews Drug Discovery, Vol. 11, No. 8, 2012, pp. 633-652.
http://dx.doi.org/10.1038/nrd3800

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