Abstract
Genetic analysis in mice has shown thai, among the cytokines that interact with the common g-chain receptor, Interleukin-7 (IL-7) is unique in its capacity to expand lymphocyte populations. However, much less is known about the potential in vivo role of IL-7 on myelold cells. No obvious abnormality in myelopoietic cells was apparent in IL-7 deficient (-/-) mice. Lymphopenic IL-7(-/-) mice were intercrossed with lymphoid deficient RAG-2(-/-) mutant mice. Adult RAG-2(-/-) but not doubly mutant IL-7( /-)/RAG-2(-/-) mice developed a severe colitis and in many cases a rectal prolapse. Routine health screening for pathogens revealed the presence of Helicobacter hepaticus (H. hepaticus) in both colonies of animals. The pathology In the RAG-2(-/-) mice was similar to that reported for naturally occuring H. hepaticus infection. In further experiments the infection was Induced by cohousing newborn animals of each genotype and by reexposure of antibiotic cured mice to the natural course of infection. WBC counts, platelets counts and serum Amyloid A were used as indices of inflammatory response. The RAG-2(-/-) mice showed significantly higher values in all parameters than the IL-7(-/-)/RAG-2(-/-) mice. Histologically RAG-2(-/-) mice showed lesions in the cecum consisting of multifocal MHC class II positive epithelial hyperplasia, ulceration with mixed inflammatory Infiltrate consisting of macrophages, PMN's and eosinophils. In contrast the cecum from IL-7(-/-)RAG-2(-/-) mice revealed no lesions. Histologically both groups of mice showed H. hepaticus in direct contact with the epithelium. These data Indicate that in the absence of lymphocytes IL-7 exacerbates an inflammatory response in the bowel after exposure to an infectious flora. IL-7 directly or indirectly activates myeloid cells or possibly NK cells and results in a pathological inflammation without obvious clearance of the suspected microbial organism.
Original language | English |
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Pages (from-to) | 136-137 |
Number of pages | 2 |
Journal | Pediatric Blood & Cancer |
Volume | 30 |
Issue number | 2 |
Publication status | Published - 1998 |
Externally published | Yes |