ArticleThe American journal of pathology2011
Chemokine receptor CXCR2 mediates bacterial clearance rather than neutrophil recruitment in a murine model of pneumonic plague.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- CXCR2 perturbation promotesJournal of medical microbiology · 2024Article
- Study on Potential Differentially Expressed Genes in Idiopathic Pulmonary Fibrosis by Bioinformatics and Next-Generation Sequencing Data Analysis.Biomedicines · 2023Article
- The immunological function of CXCR2 in the liver during sepsis.Journal of inflammation (London, England) · 2022Review
- Protection Elicited by Attenuated LiveVaccines · 2021Article
- Yersinia pestis Exploits Early Activation of MyD88 for Growth in the Lungs during Pneumonic Plague.Infection and immunity · 2019Article
- Enterobacteria and host resistance to infection.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- Induction of Type I Interferon through a Noncanonical Toll-Like Receptor 7 Pathway during Yersinia pestis Infection.Infection and immunity · 2017Article
- Review
- Mononuclear-macrophages but not neutrophils act as major infiltrating anti-leptospiral phagocytes during leptospirosis.PloS one · 2017Article
- Yersinia enterocolitica YopH-Deficient Strain Activates Neutrophil Recruitment to Peyer's Patches and Promotes Clearance of the Virulent Strain.Infection and immunity · 2016Article
- Circumventing Y. pestis Virulence by Early Recruitment of Neutrophils to the Lungs during Pneumonic Plague.PLoS pathogens · 2015Article
- Bacterial programming of host responses: coordination between type I interferon and cell death.Frontiers in microbiology · 2014Review
- A novel C5a-derived immunobiotic peptide reduces Streptococcus agalactiae colonization through targeted bacterial killing.Antimicrobial agents and chemotherapy · 2013Article
- Early-phase GVHD gene expression profile in target versus non-target tissues: kidney, a possible target?Bone marrow transplantation · 2013Article
- Staphylococcus aureus Staphopain A inhibits CXCR2-dependent neutrophil activation and chemotaxis.The EMBO journal · 2012Article
- Early sensing of Yersinia pestis airway infection by bone marrow cells.Frontiers in cellular and infection microbiology · 2012Article
- Opposing roles for interferon regulatory factor-3 (IRF-3) and type I interferon signaling during plague.PLoS pathogens · 2012Article
- Host Defense and the Airway Epithelium: Frontline Responses That Protect against Bacterial Invasion and Pneumonia.Journal of pathogens · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Pulmonary infection by Yersinia pestis causes pneumonic plague, a necrotic bronchopneumonia that is rapidly lethal and highly contagious. Acute pneumonic plague accompanies the up-regulation of pro-inflammatory cytokines and chemokines, suggesting that the host innate immune response may contribute to the development of disease. To address this possibility, we sought to understand the consequences of neutrophil recruitment during pneumonic plague, and we studied the susceptibility of C3H-HeN mice lacking the CXC chemokine KC or its receptor CXC receptor 2 (CXCR2) to pulmonary Y. pestis infection. We found that without Kc or Cxcr2, disease progression was accelerated both in bacterial growth and development of primary bronchopneumonia. When examined in an antibody clearance model, Cxcr2(-/-) mice were not protected by neutralizing Y. pestis antibodies, yet bacterial growth in the lungs was delayed in a manner associated with a neutrophil-mediated inflammatory response. After this initial delay, however, robust neutrophil recruitment in Cxcr2(-/-) mice correlated with bacterial growth and the development of fulminant pneumonic and septicemic plague. In contrast, attenuated Y. pestis lacking the conserved pigmentation locus could be cleared from the lungs in the absence of Cxcr2 indicating virulence factors within this locus may inhibit CXCR2-independent pathways of bacterial killing. Together, the data suggest CXCR2 uniquely induces host defense mechanisms that are effective against virulent Y. pestis, raising new insight into the activation of neutrophils during infection.
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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.