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Physiological Role of Macrophage Inflammatory Protein-3 Induction during Maturation of Intestinal Macrophages^1,2

Martin Hausmann^3,*, Frauke Bataille, Tanja Spoettl^*, Katja Schreiter^*, Werner Falk^*, Juergen Schoelmerich^*, Hans Herfarth^* and Gerhard Rogler^*

Departments of^* Internal Medicine I and Pathology, University of Regensburg, Regensburg, Germany

Intestinal macrophages (IMAC) are a central component in the defense of the intestinal mucosa against luminal microbes. In normal mucosa, monocytes differentiate to immunologically tolerant IMAC with a typical phenotype lacking activation markers such as CD14 and TLRs 2 and 4. CD33⁺ IMAC were isolated from normal intestinal mucosa by immunomagnetic beads. A subtractive hybridization subtracting mRNA from normal IMAC from those of in vitro differentiated macrophages was performed. IMAC differentiation was studied in multicellular spheroids (MCS). Functional assays on migration of CD45R0⁺ T cells were performed in MCS coculture models. Of 76 clones, 3 obtained by subtractive mRNA hybridization showed >99% homology to mRNA of MIP-3, indicating that this chemokine is induced in IMAC compared with in vitro differentiated macrophages. MIP-3 protein expression was confirmed in cryostat sections of normal intestinal mucosa by immunohistochemistry. IMAC in the lamina propria stained positive for MIP-3. FACS of purified IMAC clearly indicated expression of MIP-3 in these cells. In the MCS-in vitro differentiation model for IMAC, MIP-3 protein expression was absent on day 1 but detectable on day 7 of coculture, demonstrating the induction of MIP-3 during differentiation of IMAC. IMAC attracted CD45R0⁺ T cells to migrate into an MCS coculture model. In human mucosa, a close contact between IMAC and CD45R0⁺ T cells could be demonstrated. MIP-3 is induced during the differentiation of monocytes into IMAC. Our data suggest that MIP-3 expression could be involved in the recruitment of CD45R0⁺ cells into the lamina propria.

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