ArticleInfection and immunity2008
Pertussis toxin inhibits early chemokine production to delay neutrophil recruitment in response to Bordetella pertussis respiratory tract infection in mice.
Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
72 citing papers in PubMed, 95 citations in OpenAlex.
- Mechanisms of natural and vaccine-induced immunity to Bordetella pertussis.PLoS pathogens · 2026Review
- Hypofucosylation promotes pertussis toxin binding to cell surface glycococonjugates and pertussis toxin-induced intracellular ERK signaling.Glycobiology · 2026Article
- Clinical characteristics analysis of pertussis and Mycoplasma pneumoniae infection in children.Frontiers in cellular and infection microbiology · 2026Article
- Impact of pertussis vaccination on PT-IgG levels and clinical characteristics in 3-12-month-old infants with acute pertussis.European journal of pediatrics · 2025Article
- Co-infection in unvaccinated infants with acute pertussis in Western China (2018-2019): pathogen distribution and impact on disease severity.Italian journal of pediatrics · 2025Article
- Interferon lambda signaling in neutrophils enhances the pathogenesis of Bordetella pertussis infection.Journal of leukocyte biology · 2025Article
- Pertussis resurgence: epidemiological trends, pathogenic mechanisms, and preventive strategies.Frontiers in immunology · 2025Review
- Article
- Eosinophils as drivers of bacterial immunomodulation and persistence.Infection and immunity · 2024Review
- Immunization with an mRNA DTP vaccine protects against pertussis in rats.Infection and immunity · 2024Article
- Age-dependent natural killer cell and interferon γ deficits contribute to severe pertussis in infant mice.Journal of leukocyte biology · 2024Article
- Copper management strategies in obligate bacterial symbionts: balancing cost and benefit.Emerging topics in life sciences · 2024Article
- The diverse landscape of AB5-type toxins.Engineering microbiology · 2023Review
- Review
- Inhibition of Pertussis Toxin by Human α-Defensins-1 and -5: Differential Mechanisms of Action.International journal of molecular sciences · 2023Article
- The Neonatal Immune System and Respiratory Pathogens.Microorganisms · 2023Review
- Generating enhanced mucosal immunity againstFrontiers in immunology · 2023Article
- Article
- Novel murine model reveals an early role for pertussis toxin in disrupting neonatal immunity toFrontiers in immunology · 2023Article
- Pertussis toxin suppresses dendritic cell-mediated delivery of B. pertussis into lung-draining lymph nodes.PLoS pathogens · 2022Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Pertussis is an acute respiratory disease of humans caused by the bacterium Bordetella pertussis. Pertussis toxin (PT) plays a major role in the virulence of this pathogen, including important effects that it has soon after inoculation. Studies in our laboratory and other laboratories have indicated that PT inhibits early neutrophil influx to the lungs and airways in response to B. pertussis respiratory tract infection in mice. Previous in vitro and in vivo studies have shown that PT can affect neutrophils directly by ADP ribosylating G(i) proteins associated with surface chemokine receptors, thereby inhibiting neutrophil migration in response to chemokines. However, in this study, by comparing responses to wild-type (WT) and PT-deficient strains, we found that PT has an indirect inhibitory effect on neutrophil recruitment to the airways in response to infection. Analysis of lung chemokine expression indicated that PT suppresses early neutrophil recruitment by inhibiting chemokine upregulation in alveolar macrophages and other lung cells in response to B. pertussis infection. Enhancement of early neutrophil recruitment to the airways in response to WT infection by addition of exogenous keratinocyte-derived chemokine, one of the dominant neutrophil-attracting chemokines in mice, further revealed an indirect effect of PT on neutrophil chemotaxis. Additionally, we showed that intranasal administration of PT inhibits lipopolysaccharide-induced chemokine gene expression and neutrophil recruitment to the airways, presumably by modulation of signaling through Toll-like receptor 4. Collectively, these results demonstrate how PT inhibits early inflammatory responses in the respiratory tract, which reduces neutrophil influx in response to B. pertussis infection, potentially providing an advantage to the pathogen in this interaction.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.