Chemokines in the Lung by Robert M. Strieter, Steven L. Kunkel, Theodore Standiford

By Robert M. Strieter, Steven L. Kunkel, Theodore Standiford

Discusses the function of chemokines in mediating leukocyte trafficking, angiogenesis, tumor telephone metastasis, host protection, trauma-induced lung harm, and the development of AIDS within the lung. stories cytokines as usual brokers for modulating ailments that have an effect on the lung

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Mice lacking CXCR4 or its only ligand, SDF-1, have severe defects in myelopoiesis and B-lymphopoiesis, brain and heart organogenesis, and blood vessel formation in the intestinal tract. The mice die at late embryonic stages. Adoptive transfer experiments revealed that CXCR4 plays an important role in long-term lymphoid and myeloid repopulation of hematopoietic progenitor cells in adult bone marrow (98–101). Although SDF-1 is constitutively expressed in most tissues, its role in effector cell trafficking and immune surveillance is not defined.

In contrast, IL-8 (CXCL8) binds both CXCR1 and CXCR2 with similar Kds and induces neutrophil chemotaxis with a bell-shaped dose-response curve exhibiting a single optimum. Ludwig et al. demonstrated that treatment with CXCR2 monoclonal antibody suppressed the first optimum of NAP-2-induced chemotaxis, whereas CXCR1 antibody dramatically reduced the second one, suggesting that both receptors are involved in NAP-2-induced neutrophil chemotaxis, with CXCR2 rendering the neutrophils responsive to low concentrations of the chemokine, and with CXCR1 extending their responsiveness to high concentrations of NAP-2.

In Mycobacterium tuberculosis infection, CCR2Ϫ/Ϫ mice died early, had increased bacterial burden in the lung, and exhibited an early defect in macrophage recruitment and a later defect in recruitment of dendritic cells and T cells to the lung (69). CCR2 also plays a role in the pathogenesis of vascular diseases. In CCR2- Chemokine Receptors: Mechanisms and Roles 21 deficient mice, hypertension-induced macrophage infiltration of the arterial wall was virtually eliminated, and vascular hypertrophy was reduced by approximately 65% compared with wildtype animals, suggesting that CCR2 is essential for the recruitment of macrophages into the arterial wall in the setting of hypertension (70).

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