The DOI matches its Crossref record; 36 of the 36 references it cites were found in a registry or an index.
IL-17 Promotes p38 MAPK-Dependent Endothelial Activation Enhancing Neutrophil Recruitment to Sites of Inflammation
Abstract
Neutrophilic inflammation plays an important role in lung tissue destruction occurring in many chronic pulmonary diseases. Neutrophils can be recruited to sites of inflammation via the action of the cytokine IL-17. In this study, we report that IL-17RA and IL-17RC mRNA expression is significantly increased in asthmatic bronchoscopic biopsies and that these receptors are not only expressed on epithelial and inflammatory cells but also on endothelial cells. IL-17 potently stimulates lung microvascular endothelial cells to produce chemoattractants (CXCL8 and derivatives of the 5-lipoxygenase pathway) that selectively drive neutrophil but not lymphocyte chemotaxis. Moreover, IL-17 promotes endothelial activation by inducing the expression of endothelial adhesion markers (E-selectin, VCAM-1, and ICAM-1) in a p38 MAPK-dependent manner. This increased expression of adhesion molecules stimulates the trans-endothelial migration of neutrophils, as well as the transmigration of HT-29 colon carcinoma cells, suggesting a further role in promoting lung metastasis. Finally, IL-17 increased neutrophil adhesion to the endothelium in vivo as determined by intravital microscopy of mice cremaster muscle. Overall, our results demonstrate that IL-17 is a potent activator of the endothelium in vivo leading to neutrophil infiltration. Therefore, preventing neutrophil recruitment by blocking the action of IL-17 on endothelial cells may prove to be highly beneficial in diseases in which neutrophilic inflammation plays a key role.
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Cites
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T cell interleukin-17 induces stromal cells to produce proinflammatory and hematopoietic cytokines
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“Therefore, we checked whether endothelial cells synthesize CXCL8 upon IL-17 stimulation similar to what was seen with other structural cells of the airways (25).”
Resultp38 MAP-Kinases pathway regulation, function and role in human diseases
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Self-citationGlucocorticoid resistance in inflammatory diseases
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Neutrophilic Inflammation in Severe Persistent Asthma
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The role of infiltrating immune cells in dysfunctional adipose tissue
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Griffin, G. K., Newton, G., Tarrio, M. L., Bu, D.-X., Maganto-Garcia, E., Azcutia, V., Alcaide, P., Grabie, N., Luscinskas, F. W., Croce, K. J., et al. (2012) · The Journal of Immunology · doi:10.4049/jimmunol.1200385 · Cited by 364
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The Role of Th17-Related Cytokines in Atopic Dermatitis
Sugaya, M. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21041314 · Cited by 204
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Ruchti, F., & LeibundGut‐Landmann, S. (2023) · Parasite Immunology · doi:10.1111/pim.12948 · Cited by 31
Metadata
- Authors
- Roussel, L., Houle, F., Chan, C., Yao, Y., Bérubé, J., Olivenstein, R., Martin, J. G., Huot, J., Hamid, Q., Ferri, L., & Rousseau, S.
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-04
- Volume
- 184
- Issue
- 8
- Pages
- 4531-4537
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1926302666
- Cited by
- 272
- References
- 36
- FWCI
- 10.54
- Type
- journal article
- Language
- en
- Open access
- closed
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- CoChat. (2026). Citation check: IL-17 Promotes p38 MAPK-Dependent Endothelial Activation Enhancing Neutrophil Recruitment to Sites of Inflammation. https://app.cochat.ai/papers/10.4049/jimmunol.0903162
- The paper
- Roussel, L., Houle, F., Chan, C., Yao, Y., Bérubé, J., Olivenstein, R., Martin, J. G., Huot, J., Hamid, Q., Ferri, L., & Rousseau, S. (2010). IL-17 Promotes p38 MAPK-Dependent Endothelial Activation Enhancing Neutrophil Recruitment to Sites of Inflammation. The Journal of Immunology. https://doi.org/10.4049/jimmunol.0903162
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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