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Temporal Changes in Myeloid Cells in the Cervix during Pregnancy and Parturition¹

Brenda C. Timmons^*, Anna-Marie Fairhurst and Mala S. Mahendroo^2,*

^* Department of Obstetrics and Gynecology, and Department of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390

Preterm birth occurs at a rate of 12.7% in the U.S. and is the primary cause of fetal morbidity in the first year of life as well as the cause of later health problems. Elucidation of mechanisms controlling cervical remodeling is critical for development of therapies to reduce the incidence of prematurity. The cervical extracellular matrix must be disorganized during labor to allow birth, followed by a rapid repair postpartum. Leukocytes infiltrate the cervix before and after birth and are proposed to regulate matrix remodeling during cervical ripening via release of proteolytic enzymes. In the current study, flow cytometry and cell sorting were used to determine the role of immune cells in cervical matrix remodeling before, during, and after parturition. Markers of myeloid cell differentiation and activation were assessed to define phenotype and function. Tissue monocytes and eosinophils increased in the cervix before birth in a progesterone-regulated fashion, whereas macrophage numbers were unchanged. Neutrophils increased in the postpartum period. Increased mRNA expression of Csfr1 and markers of alternatively activated M2 macrophages during labor or shortly postpartum suggest a function of M2 macrophages in postpartum tissue repair. Changes in cervical myeloid cell numbers are not reflected in the peripheral blood. These data along with our previous studies suggest that myeloid-derived cells do not orchestrate processes required for initiation of cervical ripening before birth. Additionally, macrophages with diverse phenotypes (M1 and M2) are present in the cervix and are most likely involved in the postpartum repair of tissue.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work is supported by National Institutes of Health R01 HD043154 (to M.S.M.).

² Address correspondence and reprint requests to Dr. Mala S. Mahendroo, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9032. E-mail address: mala.mahendroo{at}utsouthwestern.edu

³ Abbreviations used in this paper: ECM, extracellular matrix; Arg1, arginase 1; IL-1ra, IL-1 receptor antagonist; IL-13ra1, IL-13 receptor alpha 1; NIL, not in labor; PP, postpartum; WT, wild type; IL, in labor.

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				J. M. Gonzalez, H. Xu, J. Chai, E. Ofori, and M. A. Elovitz Preterm and Term Cervical Ripening in CD1 Mice (Mus musculus): Similar or Divergent Molecular Mechanisms? Biol Reprod, December 1, 2009; 81(6): 1226 - 1232. [Abstract] [Full Text] [PDF]