title: Senescent jejunal mast cells and eosinophils in the mouse preferentially translocate to the spleen and draining lymph node, respectively, during the recovery phase of helminth infection.
abstract: Because mice infected with Trichinella spiralis experience a pronounced, but transient, mastocytosis and eosinophilia in their intestine, this disease model was used to follow the fate of senescent T cell-dependent mast cells (MCs) and eosinophils. Very few MCs or eosinophils undergoing apoptosis were found in the jejunum during the resolution phase of the infection, even though apoptotic MCs were common in the large intestine. Although the mesenteric draining lymph nodes contained large numbers of apoptotic eosinophils, MCs were rarely found at this location. During the recovery phase, large numbers of MCs were present in the spleen, and many of these cells possessed segmented nuclei. These splenic MCs were not proliferating. Although MCs from the jejunum and spleen of noninfected mice failed to express mouse MC protease (mMCP) 9, essentially all of the MCs in the jejunal submucosa and spleen of T. spiralis-infected mice expressed this serine protease during the recovery phase. The MCs in the jejunum expressed mMCP-9 before any mMCP-9-containing cells could be detected in the spleen. The fact that mMCP-9-containing MCs were detected in splenic blood vessels as these cells began to disappear from the jejunum supports the view that many jejunal MCs translocate to the spleen during the recovery phase of the infection. During this translocation process, some senescent jejunal MCs undergo nuclear segmentation. These studies reveal for the first time different exit and disposal pathways for T cell-dependent eosinophils and MCs after their expansion in the jejunum during a helminth infection.
authors.affiliation: Departments of Pathology and Medicine, Harvard Medical School, Boston, MA 02115, USA.
authors.forename: D S
authors.initials: DS
authors.lastname: Friend
authors.forename: M F
authors.initials: MF
authors.lastname: Gurish
authors.forename: K F
authors.initials: KF
authors.lastname: Austen
authors.forename: J
authors.initials: J
authors.lastname: Hunt
authors.forename: R L
authors.initials: RL
authors.lastname: Stevens
mesh_terms: D000818:Animals; D002265:Carboxylic Ester Hydrolases / Q000378:metabolism; D002461:Cell Line, Transformed; D002465:Cell Movement / Q000276:immunology*; D002467:Cell Nucleus / Q000276:immunology / Q000473:pathology; D016922:Cellular Senescence / Q000276:immunology*; D004804:Eosinophils / Q000201:enzymology / Q000276:immunology* / Q000473:pathology; D007411:Intestinal Diseases, Parasitic / Q000201:enzymology / Q000276:immunology / Q000473:pathology; D007583:Jejunum / Q000201:enzymology / Q000276:immunology* / Q000469:parasitology / Q000473:pathology; D008198:Lymph Nodes / Q000201:enzymology / Q000276:immunology* / Q000473:pathology; D008407:Mast Cells / Q000201:enzymology / Q000276:immunology* / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D020127:Recovery of Function / Q000276:immunology; D013154:Spleen / Q000201:enzymology / Q000276:immunology* / Q000473:pathology; D013601:T-Lymphocytes / Q000276:immunology; D017160:Trichinella spiralis; D014235:Trichinellosis / Q000201:enzymology / Q000276:immunology* / Q000473:pathology
chemical_list: D002265:Carboxylic Ester Hydrolases; C019873:chloroacetate esterase