HIGH LEVELS OF TUMOR NECROSIS FACTOR-ALPHA REDUCES PLACENTAL AQUAPORIN 3 EXPRESSION AND IMPAIRS in vitro TROPHOBLASTIC CELL MIGRATION

Placenta ◽  
2021 ◽  
Vol 112 ◽  
pp. e43
Author(s):  
Rinaldo Rodrigues dos Passos Junior ◽  
Raiany Alves Freitas ◽  
Julieta Reppetti ◽  
Yollyseth Medina ◽  
Vanessa Dela Justina ◽  
...  
Keyword(s):  
Cell Migration ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Trophoblastic Cell ◽  
Necrosis Factor Alpha ◽  
Aquaporin 3 ◽  
Factor Alpha ◽  
Necrosis Factor

scholarly journals Interleukin-1 and tumor necrosis factor alpha inhibit repair of the porcine meniscus in vitro

2007 ◽  
Vol 15 (9) ◽  
pp. 1053-1060 ◽  
Author(s):  
A. Hennerbichler ◽  
F.T. Moutos ◽  
D. Hennerbichler ◽  
J.B. Weinberg ◽  
F. Guilak
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

scholarly journals Cytokines regulate HIV-1 replication and lymphocyte apoptosis in vitro

2013 ◽  
Vol 94 (6) ◽  
pp. 906-910 ◽  
Author(s):  
S V Boichuk ◽  
P D Dunaev ◽  
I G Mustafin
Keyword(s):  
Flow Cytometry ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Lymphocyte Apoptosis ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Hiv 1 ◽  
Necrosis Factor

Aim. To study the ability of cytokines - interleukin-2, interleukin-7 and tumor necrosis factor alpha to induce human immunodeficiency virus type 1 (HIV-1) replication and lymphocyte apoptosis in vitro. Methods. Peripheral blood mononuclears were separated by centrifugation on a ficoll paque solution specific density gradient. Lymphocytes were cultivated in RPMI 1640 medium with addition of L-glutamine, embryonal bovine serum, antibiotics and cytokines (interleukines-2, -4, -7, tumor necrosis factor alpha). To infect the lymphocytes, a laboratory strain of HIV-1 NL4-3 (NIH ResReag. Prog., USA) was used. HIV-1 replication was assessed by р24gag viral protein level in culture supernatants (ELISA) and its cytozolic level in lymphocytes (flow cytometry). Lymphocyte apoptosis was assessed by flow cytometry using the following parameters: (1) decrease of transmembrane mitochondrial potential; (2) increase in phosphatidyl serine molecules expression. Lymphocyte activation was assessed by CD25 and HLA-DR molecules expression (flow cytometry). Results. Cytokines induce the HIV-1 replication in lymphocytes in vitro. HIV-1 replication was noted only if inactivated lymphocytes were present in the culture. At the same time, lymphocytes not expressing the classical activation markers (CD25 and HLA-DR) were present among the lymphocytes producing HIV-1 indicating the possible alternative mechanism of HIV-1 replication, not dependent on cell activation. This fact might also be an evidence of viral replication processes in the pool of latently-infected lymphocytes, not expressing the classic activation markers. The abovementioned cytokines promote apoptotic death of uninfected lymphocytes in vitro, backing up the infected cells viability and thus promoting HIV-1 replication. Conclusion. Cytokines (interleukines-2, -4, -7, tumor necrosis factor alpha) which are known as factors supporting the immune system homeostasis and immune response formation, might also play a negative role in HIV-1 pathogenesis - induce HIV-1 replication in lymphocytes and, probably, lead to reactivation of the pool of latently-infected lymphocytes, deepening the lymphopenia and leading to disease progression.

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