|Pruimboom, Ingrid - IA STATE UNIV., AMES, IA|
|Ackermann, Mark - IA STATE UNIV., AMES, IA|
Submitted to: Infection and Immunity
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: December 3, 1998
Publication Date: N/A
Interpretive Summary: Pasteurella multocida causes fowl cholera, a worldwide distributed disease of domestic and wild birds. The high mortality and morbidity that follows infection in turkeys results in significant economic losses to industry. Survival of the bacteria in the environment and its resistance to killing by monocytes and macrophages (cells of the immune system) are associated with the presence of a capsule. The capsule surrounding this bacteria is composed of a complex sugar called hyaluronic acid. In this study, we found that freshly isolated turkey blood monocytes do not bind the bacteria. However, cultures of monocytes for 6 days or exposure to different chemicals caused binding. When monocytes were treated with hyaluronic acid, binding was inhibited. We found that the material that binds P. multocida to monocytes is CD44. CD44 is probably used by P. multocida in order to invade different tissues of turkeys. The information provided by this study may give new ideas on controlling fowl cholera by interfering with the mechanisms that the bacteria uses to invade tissues.
Technical Abstract: Capsular hyaluronic acid (HA) mediates adhesion of serogroup A strains of P. multocida to elicited turkey air sac macrophages (TASM). In contrast, freshly isolated turkey peripheral blood monocytes (TPBM) do not bind serogroup A strains. Following culture of TPBM for 6 days in chameber slides, adhesion of the bacteria to TPBM increased gradually. Incubation in chamber slides coated with Entactin-Collagen IV-Laminin attachment (ECL) matrix or exposure to phorbol myristate acetate (PMA) further enhanced the adhesion of P. multocida to TPBM. Addition of HA to TPBM culture, but not Arg-Gly-Asp peptide, inhibited bacterial adherence similarly to that previously reported for TASM. Exposure of TPBM to MAb directed against HA-binding cell surface proteoglycan (CD44) decreased binding of P. multocida. Collectively, these findings indicate that P. multocida adhesion to TPBM is mediated by capsular HA and can be up- regulated by culture on ECL matrix or PMA exposure. Additionally, the findings suggest that the capsular mucopolysaccharide of serogroup A strains of P. multocida recognizes an isoform of CD44 expressed on cultured TPBM.