Immunotoxicity—The Risk is Real

Selgrade, MaryJane K.

doi:10.1093/toxsci/kfm244

Cited by 132 publications

(90 citation statements)

References 42 publications

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“…Long-term exposure to arsenic impairs lymphocyte, monocyte, and macrophage activity and, in general, affects cellular immune responses (innate immunity) in mammals, resulting in immunosuppression (Duker et al, 2005;Lemarie et al, 2006;Sakurai et al, 2006;Selgrade, 2007;Burchiel et al, 2009;Raqib et al, 2009;Qian et al, 2010). Even at low concentrations, arsenic is known to act as an immunosuppressant (Savabieasfahani et al, 1998;Stepnik et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Protective effect of curcumin against arsenic-induced apoptosis in murine splenocytesin vitro

Khan

Vala

Nabi

et al. 2011

Journal of Immunotoxicology

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Section: Introductionmentioning

confidence: 99%

Protective effect of curcumin against arsenic-induced apoptosis in murine splenocytesin vitro

Khan

Vala

Nabi

et al. 2011

Journal of Immunotoxicology

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“…Suppression of antigen-specific antibody responses is considered predictive of immunotoxicity and decreased resistance to infection in rodents (Luster et al, 1992(Luster et al, , 1993Selgrade, 1999); such alterations in murine immune function can be suggestive of health risks in similarly exposed humans (Selgrade, 2007). We previously reported that exposure to !3.75 mg PFOA/kg/day for 15 days suppressed the TDAR in C57BL/6N mice.…”

mentioning

confidence: 99%

Suppression of antigen-specific antibody responses in mice exposed to perfluorooctanoic acid: Role of PPARαand T- and B-cell targeting

DeWitt

Williams

Creech

et al. 2015

Journal of Immunotoxicology

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T-cell-dependent antibody responses (TDAR) are suppressed in female C57BL/6N mice exposed to !3.75 mg/kg of perfluorooctanoic acid (PFOA) for 15 days. To determine if suppression of humoral immunity by PFOA is peroxisome proliferator activated receptor alpha (PPAR)-dependent and if suppression is associated with specific targeting of T-or B-cells, three separate experiments were conducted: (1) female PPAR constitutive knockout (PPAR KO; B6.129S4-Ppar tm1Gonz N12) and wild-type controls (WT; C57BL/6-Tac) exposed to 0, 7.5, or 30 mg PFOA/kg for 15 days were immunized on Day 11 with a T-cell-dependent antigen and sera then collected for measures of antigen-specific IgM titers (TDAR) 5 days later; (2) female C57BL/6N WT mice exposed to 0, 0.94, 1.88, 3.75, or 7.5 mg PFOA/kg for 15 days were immunized with a T-cellindependent antigen on Day 11 and sera were then collected for analyses of antigen-specific IgM titers (TIAR) 7 days later; and (3) splenic lymphocyte phenotypes were assessed in unimmunized female C57BL/6N WT mice exposed to 0, 3.75, or 7.5 mg PFOA/kg for 10 days to investigate effects of PFOA in the absence of specific immunization. Separate groups of mice were immunized with a T-cell-dependent antigen after 11 days of exposure and splenic lymphocyte sub-populations were assessed after 13 or 15 days of exposure to assess numbers of stimulated cells. The results indicated that exposure to !1.88 mg PFOA/kg suppressed the TIAR; exposure to 30 mg PFOA/kg suppressed the TDAR in both PPAR KO and WT mice. The percentage of splenic B-cells was unchanged. Results obtained in the PPAR KO mice indicated that PPAR suppression of TDAR was independent of PPAR involvement. Suppression of the TIAR and the TDAR with minimal lymphocyte sub-population effects suggested that effects on humoral immunity are likely mediated by disruption of B-cell/plasma cell function.

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“…The percentage of 14 C PCB 77 present/total injected in shell samples varied according to embryonic day and vehicle (Table 1). Table 2 shows the MANOVA for 14 C PCB 77 uptake in a matrix of comparison of the different groups over embryonic day (1,5,10), vehicles (fatty acid and corn oil), and injection sites (air cell and albumen). Significant changes (p < 0.0001) in 14 C PCB 77 concentration confirmed movement of PCB 77 between the egg components over embryonic development, with no difference associated with vehicle type or injection site.…”

Section: Shellmentioning

confidence: 99%

Uptake of radiolabeled 3,3′,4,4′‐tetrachlorobiphenyl into Japanese quail egg compartments and embryo following air cell and albumen injection

Dean

Baltos

Marcell

et al. 2017

Enviro Toxic and Chemistry

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The avian embryo is an excellent model for testing adverse developmental effects of environmental chemicals as well as uptake and movement of xenobiotics within the egg compartments. Before incubation at embryonic day 0, 14 C 3,3 0 ,4, 4 0 -tetrachlorobiphenyl ( 14 C PCB 77) was injected into Japanese quail eggs either onto the air cell or into the albumen. All egg components were collected on embryonic day 1, 5, or 10, and concentrations of 14 C PCB 77 were measured in various egg components (shell, membrane, yolk, albumen, and embryo). The results showed measurable 14 C PCB 77 in all egg components, with changing concentrations in each egg component over the course of embryonic development. Specifically, concentrations in the shell content decreased between embryonic days 1 and 10, increased in albumen from embryonic days 1 to 5 and then decreased at embryonic day 10, and increased in both yolk and embryo from embryonic days 1 to 10. Vehicle and injection site both influenced 14 C PCB 77 allantoic fluid concentrations, with little effect on other egg components except for the inner shell membrane. The fatty acid vehicle injected into the albumen yielded the highest 14 C PCB 77 recovery. These findings demonstrate dynamic movement of toxicants throughout the egg components during avian embryonic development and a steady increase of relatively low levels of 14 C PCB 77 in the embryo compared with the yolk, albumen, and shell, suggesting that embryonic uptake (i.e., exposure) mirrors utilization of egg components for nutrition and growth during development. Environ Toxicol Chem 2018;37:126-135. C 2017 SETAC

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Immunotoxicity—The Risk is Real

Cited by 132 publications

References 42 publications

Protective effect of curcumin against arsenic-induced apoptosis in murine splenocytesin vitro

Protective effect of curcumin against arsenic-induced apoptosis in murine splenocytesin vitro

Suppression of antigen-specific antibody responses in mice exposed to perfluorooctanoic acid: Role of PPARαand T- and B-cell targeting

Uptake of radiolabeled 3,3′,4,4′‐tetrachlorobiphenyl into Japanese quail egg compartments and embryo following air cell and albumen injection

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