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Infection and Immunity, June 2001, p. 3906-3915, Vol. 69, No. 6
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.6.3906-3915.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Ureaplasma urealyticum Modulates Endotoxin-Induced Cytokine Release by Human Monocytes Derived from Preterm and Term Newborns and Adults

Winston M. Manimtim,1 Jeffrey D. Hasday,2,3,4,5,6 Lisa Hester,5 Karen D. Fairchild,1 Judith C. Lovchik,1 and Rose M. Viscardi1,*

Departments of Pediatrics,1 Medicine,2 and Pathology3 and Program of Comparative Medicine,4 University of Maryland School of Medicine, UMAB Cytokine Core Laboratory,5 and Medicine and Research Services of the Baltimore VA Medical Center,6 Baltimore, Maryland

Received 12 September 2000/Returned for modification 13 November 2000/Accepted 5 March 2001

We previously observed that Ureaplasma urealyticum respiratory tract colonization in infants with a birth weight of <= 1,250 g was associated with increases in the tracheal aspirate proinflammatory cytokines tumor necrosis factor alpha (TNF-alpha ) and interleukin-8 (IL-8) relative to the counterregulatory cytokine IL-6 during the first week of life (A. M. Patterson, V. Taciak, J. Lovchik, R. E. Fox, A. B. Campbell, and R. M. Viscardi, Pediatr. Infect. Dis. J. 17:321-328, 1998). We hypothesized that U. urealyticum alters the host immune response in the presence of a coinflammatory stimulus (e.g., bacterial infection or hyperoxia) by shifting the balance of cytokine expression towards the proinflammatory cytokines. To test this hypothesis, we compared the release of TNF-alpha , IL-8, IL-6, and IL-10 in vitro by unstimulated and U. urealyticum (with or without lipopolysaccharide [LPS])-stimulated human monocytes from adult peripheral blood and from term and preterm cord blood. U. urealyticum alone and in combination with LPS induced concentration- and development-dependent changes in cytokine release. In vitro inoculation with low-inoculum U. urealyticum (103 color-changing units [CCU]) (i) partially blocked the LPS-stimulated IL-6 release by all cells and reduced LPS-stimulated IL-10 release by preterm cells, (ii) stimulated TNF-alpha and IL-8 release by preterm cells, and (iii) augmented LPS-stimulated TNF-alpha release in all cells. In preterm cells, high-inoculum U. urealyticum (106 CCU) (i) stimulated TNF-alpha and IL-8, but not IL-6 or IL-10, release and (ii) augmented LPS-stimulated TNF-alpha and IL-8 release. High-inoculum U. urealyticum (i) stimulated release of all four cytokines in term cells and IL-8 release in adult cells and (ii) augmented LPS-induced TNF-alpha , IL-10, and IL-8 release in term cells but did not significantly affect LPS-induced cytokine release in adult cells. We speculate that U. urealyticum enhances the proinflammatory response to a second infection by blocking expression of counterregulatory cytokines (IL-6 and IL-10), predisposing the preterm infant to prolonged and dysregulated inflammation, lung injury, and impaired clearance of secondary infections.

* Corresponding author. Mailing address: Division of Neonatology, Room N5W68, University of Maryland Hospital, 22 S. Greene St., Baltimore, MD 21201. Phone: (410) 706-1913. Fax: (410) 328-1076. E-mail: rviscard{at}umaryland.edu.

Infection and Immunity, June 2001, p. 3906-3915, Vol. 69, No. 6
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.6.3906-3915.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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