Intrapulmonary T Cells Are Sufficient for Schistosoma -Induced Pulmonary Hypertension.

Autor: Fonseca Balladares, Dara C., Kassa, Biruk, Mickael, Claudia, Kumar, Rahul, Nolan, Kevin, Menezes, Thais C. F., Lee, Michael H., Lau-Xiao, Anthony M., Molofsky, Ari B., Wells, Elina, Graham, Brian B.
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Zdroj: International Journal of Molecular Sciences; Sep2024, Vol. 25 Issue 17, p9202, 14p
Abstrakt: Background: Schistosomiasis is a parasitic infection that can cause pulmonary hypertension (PH). Th2 CD4 T cells are necessary for experimental Schistosoma-PH. However, if T cells migrate to the lung to initiate, the localized inflammation that drives vascular remodeling and PH is unknown. Methods: Mice were sensitized to Schistosoma mansoni eggs intraperitoneally and then challenged using tail vein injection. FTY720 was administered, which blocks lymphocyte egress from lymph nodes. T cells were quantified using flow cytometry, PH severity via heart catheterization, and cytokine concentration through ELISA. Results: FTY720 decreased T cells in the peripheral blood, and increased T cells in the mediastinal lymph nodes. However, FTY720 treatment resulted in no change in PH or type 2 inflammation severity in mice sensitized and challenged with S. mansoni eggs, and the number of memory and effector CD4 T cells in the lung parenchyma was also unchanged. Notably, intraperitoneal Schistosoma egg sensitization alone resulted in a significant increase in intravascular lymphocytes and T cells, including memory T cells, although there was no significant change in parenchymal cell density, IL-4 or IL-13 expression, or PH. Conclusion: Blocking T cell migration did not suppress PH following Schistosoma egg challenge. Memory CD4 T cells, located in the lung intravascular space following egg sensitization, appear sufficient to cause type 2 inflammation and PH. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index
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