La recherche de Bordetella pertussis par PCR chez les parents permet de diagnostiquer la coqueluche atypique chez les jeunes nourrissons non vaccinés

Cosnes-Lambe, Cécile; Raymond, Josette; Vallet, C.; Armengaud, Jean-Baptiste; Bosdure, E.; Catalano-Pons, Charlotte; Hajje, Marie-Joelle El; Moulin, F.; Suremain, N. de; Réglier-Poupet, Hélène; Poyart, Claire; Gendrel, D.

doi:10.1016/j.lpm.2008.05.008

Cited by 2 publications

(1 citation statement)

References 15 publications

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“…Several pathogenic viruses, including adenovirus, rhinovirus and influenza virus, have been detected in the airways of patients with confirmed pertussis [9], [10], [11], [12], [13]. Infants under 4 months are at greatest risk for coinfection with respiratory syncytial virus (RSV), which can be fatal [6], [14], [15], [16], [17]. Analysis of sputum and nasal aspirates from acute and convalescent phase pertussis patients indicates that the rate of viral co-infection can be as much as 30% in adult populations and 16% in infants, and infection with more than one virus is common [1], [9], [12], [18].…”

Section: Introductionmentioning

confidence: 99%

Bordetella pertussis Infection Exacerbates Influenza Virus Infection through Pertussis Toxin-Mediated Suppression of Innate Immunity

Ayala¹,

Teijaro²,

Farber³

et al. 2011

PLoS ONE

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Pertussis (whooping cough) is frequently complicated by concomitant infections with respiratory viruses. Here we report the effect of Bordetella pertussis infection on subsequent influenza virus (PR8) infection in mouse models and the role of pertussis toxin (PT) in this effect. BALB/c mice infected with a wild-type strain of B. pertussis (WT) and subsequently (up to 14 days later) infected with PR8 had significantly increased pulmonary viral titers, lung pathology and mortality compared to mice similarly infected with a PT-deficient mutant strain (ΔPT) and PR8. Substitution of WT infection by intranasal treatment with purified active PT was sufficient to replicate the exacerbating effects on PR8 infection in BALB/c and C57/BL6 mice, but the effects of PT were lost when toxin was administered 24 h after virus inoculation. PT had no effect on virus titers in primary cultures of murine tracheal epithelial cells (mTECs) in vitro, suggesting the toxin targets an early immune response to increase viral titers in the mouse model. However, type I interferon responses were not affected by PT. Whole genome microarray analysis of gene expression in lung tissue from PT-treated and control PR8-infected mice at 12 and 36 h post-virus inoculation revealed that PT treatment suppressed numerous genes associated with communication between innate and adaptive immune responses. In mice depleted of alveolar macrophages, increase of pulmonary viral titers by PT treatment was lost. PT also suppressed levels of IL-1β, IL-12, IFN-γ, IL-6, KC, MCP-1 and TNF-α in the airways after PR8 infection. Furthermore PT treatment inhibited early recruitment of neutrophils and NK cells to the airways. Together these findings demonstrate that infection with B. pertussis through PT activity predisposes the host to exacerbated influenza infection by countering protective innate immune responses that control virus titers.

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