title: Origin of the chicken splenic reticular cells influences the effect of the infectious bursal disease virus on the extracellular matrix.
abstract: The effects of infectious bursal disease virus (IBDV) (strain F52/70) infection were studied by immunohistochemical methods on the splenic extracellular matrix (ECM). The major fibrillar components of the ECM, the type I and type III collagens and the main ECM organizing glycoproteins (laminin, tenascin and fibronectin) were monitored up to 11 days post-infection (d.p.i.). By 3 d.p.i., the collagens that form the basic scaffold of the antigen-trapping region of the spleen are destroyed, which is followed by deterioration of the glycoproteins. The ECM in the red pulp and the other regions of the white pulp (periarteriolar lymphatic sheath and germinal centre) seem to be normal. The reason for the significantly different pathological alterations in the ECM between the two regions of the spleen may be explained by the origin of the reticular cells. The reticular cells in the antigen-trapping zone and other splenic regions are of haemopoietic and mesenchymal origins, respectively. Possibly, the reticular cells of the haemopoietic origin are more susceptible for the IBDV infection than the mesenchymal ones. Development of the antigen-trapping, B-cell-dependent zone of the splenic white pulp precedes that of the periarteriolar lymphatic sheath and germinal centre, which suggests that this region may contribute to B-cell maturation. Damage of the ECM in the antigen-trapping zones results in impairment of tissue organization, which may contribute to the permanent immunosuppression.
authors.affiliation: Department of Human Morphology and Developmental Biology, Semmelweis University, Túzoltó u 58, Budapest, Hungary.
authors.forename: E
authors.initials: E
authors.lastname: Bíró
authors.forename: K
authors.initials: K
authors.lastname: Kocsis
authors.forename: N
authors.initials: N
authors.lastname: Nagy
authors.forename: D
authors.initials: D
authors.lastname: Molnár
authors.forename: S
authors.initials: S
authors.lastname: Kabell
authors.forename: V
authors.initials: V
authors.lastname: Palya
authors.forename: I
authors.initials: I
authors.lastname: Oláh
mesh_terms: D000818:Animals; D001402:B-Lymphocytes; D001665:Binding Sites; D018175:Birnaviridae Infections / Q000662:veterinary* / Q000821:virology; D002060:Bursa of Fabricius / Q000821:virology; D002465:Cell Movement; D002645:Chickens / Q000821:virology*; D024042:Collagen Type I / Q000032:analysis / Q000378:metabolism; D024061:Collagen Type III / Q000032:analysis / Q000378:metabolism; D005109:Extracellular Matrix / Q000378:metabolism / Q000648:ultrastructure / Q000821:virology*; D005353:Fibronectins / Q000032:analysis; D006023:Glycoproteins / Q000032:analysis; D006412:Hematopoietic Stem Cells / Q000166:cytology / Q000821:virology; D007150:Immunohistochemistry / Q000662:veterinary; D007243:Infectious bursal disease virus / Q000472:pathogenicity*; D007797:Laminin / Q000032:analysis; D059630:Mesenchymal Stem Cells / Q000166:cytology / Q000821:virology; D008854:Microscopy, Electron / Q000662:veterinary; D012155:Reticulin / Q000032:analysis / Q000648:ultrastructure; D013047:Specific Pathogen-Free Organisms; D013154:Spleen / Q000166:cytology / Q000648:ultrastructure / Q000821:virology*; D019063:Tenascin / Q000032:analysis
chemical_list: D024042:Collagen Type I; D024061:Collagen Type III; D005353:Fibronectins; D006023:Glycoproteins; D007797:Laminin; D012155:Reticulin; D019063:Tenascin