A “possible” involvement of TNF-alpha in apoptosis induction in peripheral blood lymphocytes of cats with feline infectious peritonitis

Takano, Tomomi; Hohdatsu, Tsutomu; Hashida, Yoshikiyo; Kaneko, Yasuhiro; Tanabe, Masao; Koyama, Hiroyuki

doi:10.1016/j.vetmic.2006.08.033

Cited by 59 publications

(85 citation statements)

References 27 publications

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“…Lymphopenia is commonly present in FIP cats in both the T and B cell population in all immunological compartments (blood, LN and spleen) (Haagmans et al, 1996;Takano et al, 2007). This was verified in our setup through staining of CD21 and CD3 molecules.…”

Section: Discussionsupporting

confidence: 76%

“…This depletion might be the result of apoptosis, like was found for T and B cells. Roles for several apoptosis-inducing factors (TNF-a, TRAIL and Fas ligand) have already been proposed (Takano et al, 2007), but need to be verified. In addition to cell frequency, cell phenotype also plays an important role in the functionality of a particular cell type (Morishima et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

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Suppression of NK cells and regulatory T lymphocytes in cats naturally infected with feline infectious peritonitis virus

Vermeulen

Devriendt

Olyslaegers

et al. 2013

Veterinary Microbiology

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A strong cell-mediated immunity (CMI) is thought to be indispensable for protection against infection with feline infectious peritonitis virus (FIPV) in cats. In this study, the role of natural killer (NK) cells and regulatory T cells (Tregs), central players in the innate and adaptive CMI respectively, was examined during natural FIPV infection. When quantified, both NK cells and Tregs were drastically depleted from the peripheral blood, mesenteric lymph node (LN) and spleen in FIP cats. In contrast, mesentery and kidney from FIP cats did not show any difference when compared to healthy non-infected control animals. In addition, other regulatory lymphocytes (CD4+CD25-Foxp3+ and CD3+CD8+Foxp3+) were found to be depleted from blood and LN as well. Phenotypic analysis of blood-derived NK cells in FIP cats revealed an upregulation of activation markers (CD16 and CD25) and migration markers (CD11b and CD62L) while LN-derived NK cells showed upregulation of only CD16 and CD62L. LN-derived NK cells from FIPV-infected cats were also significantly less cytotoxic when compared with healthy cats. This study reveals for the first time that FIPV infection is associated with severe suppression of NK cells and Tregs, which is reflected by cell depletion and lowered cell functionality (only NK cells). This will un-doubtfully lead to a reduced capacity of the innate immune system (NK cells) to battle FIPV infection and a decreased capacity (Tregs) to suppress the immunopathology typical for FIP. However, these results will also open possibilities for new therapies targeting specifically NK cells and Tregs to enhance their numbers and/or functionality during FIPV infection.

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Section: Discussionsupporting

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Suppression of NK cells and regulatory T lymphocytes in cats naturally infected with feline infectious peritonitis virus

Vermeulen

Devriendt

Olyslaegers

et al. 2013

Veterinary Microbiology

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“…The primer sequences are shown in Table 1. PCR was performed using the method of Takano et al (2007a). The band density was quantified under appropriate UV exposure by video densitometry using Scion Image software (Scion Corporation, U.S.A.).…”

Section: Determination Of Levels Of Feline Gapdh Mrna Vegf Mrna Andmentioning

confidence: 99%

Vascular endothelial growth factor (VEGF), produced by feline infectious peritonitis (FIP) virus-infected monocytes and macrophages, induces vascular permeability and effusion in cats with FIP

et al. 2011

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Feline infectious peritonitis virus (FIPV) causes a fatal disease called FIP in Felidae. The effusion in body cavity is commonly associated with FIP. However, the exact mechanism of accumulation of effusion remains unclear. We investigated vascular endothelial growth factor (VEGF) to examine the relationship between VEGF levels and the amounts of effusion in cats with FIP. Furthermore, we examined VEGF production in FIPV-infected monocytes/macrophages, and we used feline vascular endothelial cells to examine vascular permeability induced by the culture supernatant of FIPV-infected macrophages. In cats with FIP, the production of effusion was related with increasing plasma VEGF levels. In FIPV-infected monocytes/macrophages, the production of VEGF was associated with proliferation of virus. Furthermore, the culture supernatant of FIPV-infected macrophages induced hyperpermeability of feline vascular endothelial cells. It was suggested that vascular permeability factors, including VEGF, produced by FIPV-infected monocytes/macrophages might increase the vascular permeability and the amounts of effusion in cats with FIP.

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“…cDNA was amplified by PCR using specific primers as shown in Table 3. PCR was performed using the method of Takano et al (2007a). Band density was quantified under appropriate UV exposure by video densitometry using Image J software (NIH, U.S.A.).…”

Section: Determination Of Feline Cytokine Mrna and Fcov N Gene Expresmentioning

confidence: 99%

Effect of chloroquine on feline infectious peritonitis virus infection in vitro and in vivo

et al. 2013

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Feline infectious peritonitis (FIP) is a feline coronavirus-induced fatal disease in domestic and wild cats. Several studies have investigated potential treatments for FIP. However, there have been no reports on agents that have exhibited a therapeutic effect. Recently, chloroquine has been reported to antiviral effect. We investigated whether chloroquine can be used to treat FIP in vitro and in vivo. It was demonstrated that chloroquine has inhibitory effect against the replication of FIPV and anti-inflammatory effect in vitro. In vivo study using cats with experimentally induced FIP, the clinical score of chloroquine-treatment groups were better than in chloroquine-untreated group. However, alanine aminotransferase levels increased in the chloroquine-treated groups. It will be necessary to further investigate the possibility of FIP treatment with a combination of chloroquine and other agents.

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A “possible” involvement of TNF-alpha in apoptosis induction in peripheral blood lymphocytes of cats with feline infectious peritonitis

Cited by 59 publications

References 27 publications

Suppression of NK cells and regulatory T lymphocytes in cats naturally infected with feline infectious peritonitis virus

Suppression of NK cells and regulatory T lymphocytes in cats naturally infected with feline infectious peritonitis virus

Vascular endothelial growth factor (VEGF), produced by feline infectious peritonitis (FIP) virus-infected monocytes and macrophages, induces vascular permeability and effusion in cats with FIP

Effect of chloroquine on feline infectious peritonitis virus infection in vitro and in vivo

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