Lack of IL-10 Release from Human Polymorphonuclear Leukocytes

Lee,  Sung Woo; Kim,  Su Jin; Yoon,  Young Hoon; Jung,  In Chul; Lee,  Be Ahn; Moon,  Sung Woo; Jung,  Sang Hun; Hong,  Suk Hyun; Chun,  Chung Min; Kim,  Nak Hoon; Hong,  Yun Sik

J Korean Soc Emerg Med > Volume 13(4); 2002 > Article

Original Article

Journal of The Korean Society of Emergency Medicine 2002;13(4): 411-415.

Lack of IL-10 Release from Human Polymorphonuclear Leukocytes

Sung Woo Lee, Su Jin Kim, Young Hoon Yoon, In Chul Jung, Be Ahn Lee, Sung Woo Moon, Sang Hun Jung, Suk Hyun Hong, Chung Min Chun, Nak Hoon Kim, Yun Sik Hong

Department of Emergency Medicine, College of Medicine, Korea University, Seoul, Korea. kuedlee@korea.ac.kr

ABSTRACT

PURPOSE:
Polymorphonuclear leukocytes (PMNs) are the first line of cellular response for host defense during acute inflammation. The ability of PMNs to produce and release numerous pro-inflammatory cytokines is now estabilished and plays an important role in triggering and maintaining the inflammatory response. We studied the autocrine downregulation of this process by invesgating the potential production by human PMNs of the major anti-inflammatory cytokine, interleukine 10 (IL-10).
METHODS:
Human PMNs were isolated from the peripheral blood of health volunteers by using the modified boyum method. Human PMNs were incubated at 37 degrees Cwith and without formyl Met-Leu-Phe (fMLP) for 30 minute, 2 hours, 4 hours, and 20 hours. The level of IL-10 was determined in each of the cell-free supernatants by using the enzyme linked immunosorbent assay (ELISA) method.
RESULTS:
Non-stimulated PMNs generated 1.40 +/- 1.791pg/mL to 3.46 +/- 1.607 pg/mL of IL-10 over the time course. Stimulation with fMLP resulted in an increase in the constitutive PMN-derived IL-10 by 2.74 +/- 0.762 pg/mL, 1.27 +/- 0.262 pg/mL, 1.19 +/- 0.364 pg/mL, and 2.44 +/- 1.317 pg/mL at 30 min, 2 hr, 4 hr, and 20 hr after stimulation, respectively, but these increases were not statiscally significant.
CONCLUSION:
Human PMNs seem unable to induce release of the most potent anti-inflammatory cytokine, IL-10, and down-regulate inflammatory response due to the autocrine mechanism. This could partly account for the persistence of local inflammation, when PMNs are the main infiltrating cells.

Key words: Polymorphonuclear leukocytes, Interleukine-10, Formyl-methionyl-leucyl-phenylalanine (fMLP)