Immunoglobulin A-Mediated Protection againstBordetella pertussisInfection
| Autor: | Sandra M. M. Hellwig, Annemiek B. van Spriel, Frits R. Mooi, Jan G. J. van de Winkel, Joop F. P. Schellekens |
|---|---|
| Rok vydání: | 2001 |
| Předmět: |
Male
Immunoglobulin A Bordetella pertussis Neutrophils Whooping Cough Immunology Antigen presentation Mice Transgenic Receptors Fc Pertussis toxin Microbiology Mice Immune system Phagocytosis Antigens CD Immunity Animals Humans Host Response and Inflammation biology biology.organism_classification Antibodies Bacterial Mice Inbred C57BL Bacterial adhesin Infectious Diseases biology.protein Female Parasitology Antibody |
| Zdroj: | Infection and Immunity. 69:4846-4850 |
| ISSN: | 1098-5522 0019-9567 |
| DOI: | 10.1128/iai.69.8.4846-4850.2001 |
| Popis: | The gram-negative bacterium Bordetella pertussis is the causative agent of pertussis (whooping cough). B. pertussis expresses various virulence factors, including adhesins and toxins, which all play a role in pathogenesis. B. pertussis colonizes the respiratory tract using adhesins specific for ciliated cells of the respiratory epithelium. Toxins are produced and are involved in disrupting host immune responses (21). The mechanisms underlying immunity to B. pertussis are incompletely understood. In murine infection models, protection against infection was obtained upon passive transfer of anti-B. pertussis antibodies (8, 10, 23). In addition, protective effects of T helper 1 cells (2, 16) and B cells (14) have been observed, indicating that antibodies, B cells, and T cells are involved in protective immunity. Protection against bacterial infections depends on effector activities by phagocytic cells. Elimination of bacteria involves opsonization with antibodies and recognition by certain receptors that may result in phagocytosis, bacterial killing, and antigen presentation. Upon B. pertussis infection in humans, antibody levels rise, and high levels in acute-phase sera have been associated with a lower likelihood of acquiring pertussis (3, 5, 24). Anti-B. pertussis antibodies consist of different isotypes, including immunoglobulin A (IgA) (19, 37). B. pertussis is noninvasive and is found exclusively on mucosa of the respiratory tract. Since IgA represents the predominant antibody isotype at mucosal surfaces, a role for IgA in anti-B. pertussis mechanisms is possible. IgA is generally believed to function by neutralizing and agglutinating pathogens or by preventing their attachment to mucosal surfaces (4, 12). The role of IgA, however, may be much broader because of effector functions induced by binding to IgA receptors. The prototypic IgA receptor (FcαRI [CD89]) is found exclusively on cells of the myeloid lineage: monocytes, macrophages, neutrophils, and eosinophils (13, 15, 17). Increasing evidence shows that FcαRI exhibits potent proinflammatory capacities. FcαRI cross-linking readily induces phagocytosis, degranulation, respiratory burst, antibody-dependent cellular cytotoxicity, and the release of proinflammatory cytokines (31). The aim of the present study was to evaluate IgA-mediated effector functions against B. pertussis by studying the interaction of IgA-coated B. pertussis with human polymorphonuclear leukocytes (PMNL). In addition, experiments were performed with transgenic (Tg) mice expressing the human FcαRI (28). There is no known homologue of FcαRI in mice, and CD89-Tg mice have been used to study the in vivo role of human FcαRI (29). We demonstrate that anti-B. pertussis IgA exhibits bactericidal effector function via facilitation of binding, phagocytosis, and killing of B. pertussis involving FcαRI. |
| Databáze: | OpenAIRE |
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