ArticleThe American journal of pathology2010
Aberrant inflammatory response to Streptococcus pyogenes in mice lacking myeloid differentiation factor 88.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- Article
- The burden of group AiScience · 2025Review
- Negative Cross-Talk between TLR2/4-Independent AMPKα1 and TLR2/4-Dependent JNK RegulatesJournal of immunology (Baltimore, Md. : 1950) · 2022Article
- Pilus proteins from Streptococcus pyogenes stimulate innate immune responses through Toll-like receptor 2.Immunology and cell biology · 2022Article
- Host-to-Host Group A Streptococcus Transmission Causes Infection of the Lamina Propria but Not Epithelium of the Upper Respiratory Tract in MyD88-Deficient Mice.Infection and immunity · 2022Article
- AmBio · 2021Article
- Colonization of the Murine Oropharynx by Streptococcus pyogenes Is Governed by the Rgg2/3 Quorum Sensing System.Infection and immunity · 2020Article
- HECT E3 Ubiquitin Ligase-Regulated Txnip Degradation Facilitates TLR2-Mediated Inflammation During Group A Streptococcal Infection.Frontiers in immunology · 2019Article
- Crucial Role of Nucleic Acid Sensing via Endosomal Toll-Like Receptors for the Defense ofFrontiers in immunology · 2019Article
- Association of matrix metalloproteinase 3 and endogenous inhibitors with inflammatory markers in mitral valve disease and calcification.Molecular biology reports · 2018Article
- Lipoteichoic acid anchor triggers Mincle to drive protective immunity against invasive group AProceedings of the National Academy of Sciences of the United States of America · 2018Article
- Dextromethorphan Attenuates NADPH Oxidase-Regulated Glycogen Synthase Kinase 3β and NF-κB Activation and Reduces Nitric Oxide Production in Group A Streptococcal Infection.Antimicrobial agents and chemotherapy · 2018Article
- Streptococcal M protein promotes IL-10 production by cGAS-independent activation of the STING signaling pathway.PLoS pathogens · 2018Article
- Group A Streptococcus encounters with host macrophages.Future microbiology · 2018Review
- Innate immune response to Streptococcus pyogenes depends on the combined activation of TLR13 and TLR2.PloS one · 2015Article
- Host responses to group a streptococcus: cell death and inflammation.PLoS pathogens · 2014Review
- Responses of innate immune cells to group A Streptococcus.Frontiers in cellular and infection microbiology · 2014Review
- Article
- Experimental and natural infections in MyD88- and IRAK-4-deficient mice and humans.European journal of immunology · 2012Review
- Intrapulmonary administration of leukotriene B(4) augments neutrophil accumulation and responses in the lung to Klebsiella infection in CXCL1 knockout mice.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several in vitro studies have emphasized the importance of toll-like receptor/myeloid differentiation factor 88 (MyD88) signaling in the inflammatory response to Streptococcus pyogenes. Since the extent of inflammation has been implicated in the severity of streptococcal diseases, we have examined here the role of toll-like receptor/MyD88 signaling in the pathophysiology of experimental S. pyogenes infection. To this end, we compared the response of MyD88-knockout (MyD88(-/-)) after subcutaneous inoculation with S. pyogenes with that of C57BL/6 mice. Our results show that MyD88(-/-) mice harbored significantly more bacteria in the organs and succumbed to infection much earlier than C57BL/6 animals. Absence of MyD88 resulted in diminished production of inflammatory cytokines such as interleukin-12, interferon-gamma, and tumor necrosis factor-alpha as well as chemoattractants such as monocyte chemotactic protein-1 (MCP-1) and Keratinocyte-derived chemokine (KC), and hampered recruitment of effector cells involved in bacterial clearance (macrophages and neutrophils) to the infection site. Furthermore, MyD88(-/-) but not C57BL/6 mice exhibited a massive infiltration of eosinophils in infected organs, which can be explained by an impaired production of the regulatory chemokines, gamma interferon-induced monokine (MIG/CXCL9) and interferon-induced protein 10 (IP-10/CXCL10), which can inhibit transmigration of eosinophils. Our results indicate that MyD88 signaling targets effector cells to the site of streptococcal infection and prevents extravasation of cells that can induce tissue damage. Therefore, MyD88 signaling may be important for shaping the quality of the inflammatory response elicited during infection to ensure optimal effector functions.
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