Bordatella pertussisRespiratory Infection in Children Is Associated with Preferential Activation of Type 1 T Helper Cells

Abstract

The mechanism of protective immunity against Bordetella pertussis generated following recovery from whooping cough in childhood has not yet been elucidated. Studies with a murine respiratory infection model have indicated that cellular immunity, mediated by Th1 cells, plays a role in the clearance of a primary infection with B. pertussis and in protection against subsequent challenge. In the present study, the induction of B. pertussis-specific Th cell subsets in children was examined. Peripheral blood mononuclear cells from B. pertussis-infected or convalescent children proliferated and secreted cytokines following antigen stimulation in vitro. In contrast, responses were weak or undetectable in the majority of children who had not been infected or vaccinated. In all cases, responding T cells produced interferon-gamma but low or undetectable interleukin-5. The findings suggest that Th1 cells may play a role in protective immunity generated following infection with B. pertussis in children.

Toll-Like Receptor 4-Mediated Innate IL-10 Activates Antigen-Specific Regulatory T Cells and Confers Resistance toBordetella pertussisby Inhibiting Inflammatory Pathology

“…These inflammatory mediators play important roles in leukocyte recruitment in the protective cellular response to bacterial infections (25)(26)(27). B. pertussis can be taken up by macrophages and neutrophils, and it has been firmly established that Th1 cells can mediate protective cellular immunity to B. pertussis (15,16). Rapid infiltration of neutrophils into the lungs was demonstrated following B. pertussis challenge of naive BALB/c (27) and C3H/HeN mice (present study), but this early cellular influx was not observed in TLR4-defective mice.…”

“…pertussis is a Gram-negative bacterium that causes whooping cough, a protracted respiratory disease in young children. Recovery from infection in both children and mice is associated with the development of B. pertussis-specific Th1 cells (15,16). Adoptive transfer of Th1 cells from convalescent mice can confer protection (15), and IFN-␥ receptor knockout mice develop lethal disseminating infection (17).…”

Modulation of Innate and Acquired Immune Responses by Escherichia coli Heat-Labile Toxin: Distinct Pro- and Anti-Inflammatory Effects of the Nontoxic AB Complex and the Enzyme Activity

“…In contrast, the completely nontoxic mutant, which retained receptor binding activity, did not suppress B. pertussis-specific IFN-␥ production and either had no significant effect or enhanced the rate of clearance of B. pertussis from the lungs. Infection of mice (20) or humans (30) with B. pertussis results in the selective induction of Th1 cells, and these cells mediate bacterial clearance and confer immunity against subsequent infection. We observed suppression of IFN-␥ production, enhancement of IL-4 and IL-5, reversal of the IgG1/IgG2a ratio, and exacerbation of infection in mice treated with LTR72 before respiratory infection with B. pertussis.…”

Assessing vaccine effectiveness of publicly funded vaccination programs in Queensland

“…Both CD4 (Th1, Th2, and Th17) and CD8 T cells specific to various pertussis toxins are produced after natural infection or vaccination (174,175). In particular, CD4 (Th) cells are central to effective immune responses to pertussis and are vital to immune functions other than promoting antibody production (167).…”

“…Further, T cell deficient mice can clear pertussis infection if passively transfused with pertussis-primed CD4 cells, but not with CD8 cells (176). Pertussis infection induces a potent Th1 response that is necessary to clear infection (175). In a baboon model, both those primed with wP and previously infected animals had a strong pertussis specific Th17 and Th1 response, whereas those vaccinated with aP had a Th1/Th2 response.…”