scholarly journals Immunoglobulin A-Mediated Protection against Bordetella pertussis Infection

2001 ◽  
Vol 69 (8) ◽  
pp. 4846-4850 ◽  
Author(s):  
Sandra M. M. Hellwig ◽  
Annemiek B. van Spriel ◽  
Joop F. P. Schellekens ◽  
Frits R. Mooi ◽  
Jan G. J. van de Winkel
Keyword(s):  
Transgenic Mice ◽  
Bordetella Pertussis ◽  
Polymorphonuclear Leukocytes ◽  
Whooping Cough ◽  
Immunoglobulin A ◽  
Pertussis Infection ◽  
Bacterial Killing ◽  
Effector Functions ◽  
Human Polymorphonuclear Leukocytes

ABSTRACT Infection with Bordetella pertussis, the causative agent of pertussis (whooping cough) in humans, is followed by the production of antibodies of several isotypes, including immunoglobulin A (IgA). Little is known, however, about the role of IgA in immunity against pertussis. Therefore, we studied targeting ofB. pertussis to the myeloid receptor for IgA, FcαRI (CD89), using either IgA purified from immune sera of pertussis patients or bispecific antibodies directed against B. pertussis and FcαRI (CD89 BsAb). Both IgA and CD89 BsAb facilitated FcαRI-mediated binding, phagocytosis, and bacterial killing by human polymorphonuclear leukocytes (PMNL) and PMNL originating from human FcαRI-transgenic mice. Importantly, FcαRI targeting resulted in enhanced bacterial clearance in lungs of transgenic mice. These data support the capacity of IgA to induce anti-B. pertussis effector functions via the myeloid IgA receptor, FcαRI. Increasing the amount of IgA antibodies induced by pertussis vaccines may result in higher vaccine efficacy.

scholarly journals Strain-Dependent Role of BrkA during Bordetella pertussis Infection of the Murine Respiratory Tract

2004 ◽  
Vol 72 (10) ◽  
pp. 5919-5924 ◽  
Author(s):  
Kelly D. Elder ◽  
Eric T. Harvill
Keyword(s):  
Respiratory Tract ◽  
Bordetella Pertussis ◽  
Whooping Cough ◽  
Single Gene ◽  
Wild Type ◽  
Pertussis Infection ◽  
Redundant Functions

ABSTRACT Bordetella pertussis, the causative agent of whooping cough, expresses many virulence factors believed to be involved in infection and disease progression. While these factors as a group are required for infection, deletion of individual virulence factor genes generally has limited effects on the ability of B. pertussis to efficiently infect the respiratory tract of mice, suggesting they may perform noncritical or redundant functions. We have recently observed that a B. pertussis strain, putatively with a mutation of a single gene, brkA, results in a severe defect in vivo. Although BrkA has been shown to be required for B. pertussis to resist complement-mediated killing in vitro, the relevance of these findings to the in vivo role of BrkA during infection has not been examined. Transducing this mutation into multiple wild-type B. pertussis strains allowed us to confirm the in vitro phenotype of reduced resistance to serum complement. All ΔbrkA mutants were increased in their sensitivity to complement in vitro, both in the presence and absence of antibodies. However, these strains differed substantially in their phenotypes in vivo. ΔbrkA mutants of recent clinical isolates were indistinguishable from wild-type strains in their efficient infection of respiratory organs, suggesting that the function of BrkA in these strains is noncritical or redundant. In contrast, multiple ΔbrkA strains derived from Tohama I were severely defective during the first week postinoculation compared to their wild-type parent. This defect was present even in complement-deficient mice, revealing a complement-independent phenotype for the ΔbrkA mutant in respiratory tract infection.

Role of myeloperoxidase in respiratory burst of human polymorphonuclear leukocytes

Inflammation ◽  
1985 ◽  
Vol 9 (1) ◽  
pp. 21-31 ◽  
Author(s):  
P. Dri ◽  
M. R. Soranzo ◽  
R. Cramer ◽  
R. Menegazzi ◽  
V. Miotti ◽  
...  
Keyword(s):  
Respiratory Burst ◽  
Polymorphonuclear Leukocytes ◽  
Human Polymorphonuclear Leukocytes

Triggering receptor expressed on myeloid cells-1 (TREM-1) contributes to Bordetella pertussis inflammatory pathology

2021 ◽  
Author(s):  
Danisha Gallop ◽  
Karen Scanlon ◽  
Jeremy Ardanuy ◽  
Alexander B. Sigalov ◽  
Nicholas H. Carbonetti ◽  
...  
Keyword(s):  
Bordetella Pertussis ◽  
Inflammatory Responses ◽  
Whooping Cough ◽  
Pulmonary Inflammation ◽  
Myeloid Cells ◽  
Cell Surface Receptor ◽  
Bacterial Burden ◽  
Emerging Pathogens ◽  
Pertussis Infection ◽  
Bacterial Control

Whooping cough (pertussis) is a severe pulmonary infectious disease caused by the bacteria Bordetella pertussis . Pertussis infects an estimated 24 million people annually, resulting in >150,000 deaths. The NIH placed pertussis on the list of emerging pathogens in 2015. Antibiotics are ineffective unless administered before the onset of the disease characteristic cough. Therefore, there is an urgent need for novel pertussis therapeutics. We have shown that sphingosine-1-phosphate receptor (S1PR) agonists reduce pertussis inflammation, without increasing bacterial burden. Transcriptomic studies were performed to identify this mechanism and allow for the development of pertussis therapeutics which specifically target problematic inflammation without sacrificing bacterial control. These data suggested a role for triggering receptor expressed on myeloid cells-1 (TREM-1). TREM-1 cell surface receptor functions as an amplifier of inflammatory responses. Expression of TREM-1 is increased in response to bacterial infection of mucosal surfaces. In mice, B. pertussis infection results in TLR9-dependent increased expression of TREM-1 and its associated cytokines. Interestingly, S1PR agonists dampen pulmonary inflammation and TREM-1 expression. Mice challenged intranasally with B. pertussis and treated with ligand-dependent (LP17) and ligand-independent (GF9) TREM-1 inhibitors showed no differences in bacterial burden and significantly reduced TNF-α and CCL-2 expression compared to controls. Mice receiving TREM-1 inhibitors showed reduced pulmonary inflammation compared to controls indicating that TREM-1 promotes inflammatory pathology, but not bacterial control, during pertussis infection. This implicates TREM-1 as a potential therapeutic target for the treatment of pertussis.

Could this be whooping cough?

2018 ◽  
Vol 35 (10) ◽  
pp. 639-642 ◽  
Author(s):  
Patrick Nee ◽  
Elaine Weir ◽  
Madhur Vardhan ◽  
Ankita Vaidya
Keyword(s):  
Young Children ◽  
Clinical Features ◽  
Respiratory Infection ◽  
Bordetella Pertussis ◽  
Whooping Cough ◽  
Pertussis Infection ◽  
Respiratory Disorders ◽  
Very Young Children ◽  
Geographical Regions ◽  
Serious Disease

Whooping cough is a notifiable bacterial respiratory infection caused by Bordetella pertussis. It may produce serious disease, especially in immunocompromised individuals and very young children. The number of reported cases increases in the winter months and the incidence peaks every 4–5 years. However, this periodicity is variable and is inconsistent between different geographical regions. Bordetella pertussis infection (BPI) may be underdiagnosed because of its seasonality and the fact that clinical features may be indistinguishable from other respiratory disorders in the paediatric ED setting. Treatment with antibiotics reduces the period of infectivity but may not shorten the illness. This review discusses the epidemiology of the disease, its clinical features, diagnosis, treatment and the disposition of patients with BPI.

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