Limits...
Allicin enhances host pro-inflammatory immune responses and protects against acute murine malaria infection.

Feng Y, Zhu X, Wang Q, Jiang Y, Shang H, Cui L, Cao Y - Malar. J. (2012)

Bottom Line: This effect is at least partially due to improved host immune responses.The absolute numbers of CD4+ T cells, DCs and macrophages were significantly higher in allicin-treated mice.In addition, allicin promoted the maturation of CD11c+ DCs, whereas it did not cause major changes in IL-4 and the level of anti-inflammatory cytokine IL-10.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Immunology, College of Basic Medical Sciences, China Medical University, Shenyang, Liaoning, China.

ABSTRACT

Background: During malaria infection, multiple pro-inflammatory mediators including IFN-γ, TNF and nitric oxide (NO) play a crucial role in the protection against the parasites. Modulation of host immunity is an important strategy to improve the outcome of malaria infection. Allicin is the major biologically active component of garlic and shows anti-microbial activity. Allicin is also active against protozoan parasites including Plasmodium, which is thought to be mediated by inhibiting cysteine proteases. In this study, the immunomodulatory activities of allicin were assessed during acute malaria infection using a rodent malaria model Plasmodium yoelii 17XL.

Methods: To determine whether allicin modulates host immune responses against malaria infection, mice were treated with allicin after infection with P. yoelii 17XL. Mortality was checked daily and parasitaemia was determined every other day. Pro-inflammatory mediators and IL-4 were quantified by ELISA, while NO level was determined by the Griess method. The populations of dendritic cells (DCs), macrophages, CD4+ T and regulatory T cells (Treg) were assessed by FACS.

Results: Allicin reduced parasitaemia and prolonged survival of the host in a dose-dependent manner. This effect is at least partially due to improved host immune responses. Results showed that allicin treatment enhanced the production of pro-inflammatory mediators such as IFN-γ, TNF, IL-12p70 and NO. The absolute numbers of CD4+ T cells, DCs and macrophages were significantly higher in allicin-treated mice. In addition, allicin promoted the maturation of CD11c+ DCs, whereas it did not cause major changes in IL-4 and the level of anti-inflammatory cytokine IL-10.

Conclusions: Allicin could partially protect host against P. yoelii 17XL through enhancement of the host innate and adaptive immune responses.

Show MeSH

Related in: MedlinePlus

Effects of allicin treatment on parasitaemia and survival of P. yoelii 17XL infected mice. Mice were treated with two doses of allicin (3 and 9 mg/kg) and PBS (control group) for successive three days after  P. yoelii 17 XL infection. Parasitaemia was calculated by counting the number of parasite-infected erythrocytes per 1,000 erythrocytes. Mortality was monitored daily. Results are presented as arithmetic mean of three mice per group ± the standard error of the mean (SEM). ##, significant difference (P < 0.001) compared to the control group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC3472178&req=5

Figure 1: Effects of allicin treatment on parasitaemia and survival of P. yoelii 17XL infected mice. Mice were treated with two doses of allicin (3 and 9 mg/kg) and PBS (control group) for successive three days after P. yoelii 17 XL infection. Parasitaemia was calculated by counting the number of parasite-infected erythrocytes per 1,000 erythrocytes. Mortality was monitored daily. Results are presented as arithmetic mean of three mice per group ± the standard error of the mean (SEM). ##, significant difference (P < 0.001) compared to the control group.

Mentions: The P. yoelii 17XL strain is highly virulent to BALB/c mice and causes lethal infection. In the control group, parasitaemia rose sharply and reached a peak level (51.8%) on day 5 PI (Figure 1A) and all mice died by day 7 (Figure 1B). In contrast, three-day oral allicin treatments at two dosages significantly reduced the day 5 parasitaemias (27.1% and 32.6% for the 3 and 9 mg/kg groups, respectively). Further decline of the parasitaemia was noticed on day 7 PI in both allicin treatment groups (Figure 1A). Consistent with an earlier observation on the effect of allicin on Plasmodium berghei erythrocytic infection[30], allicin treatments at both dosages significantly extended the survival time of infected mice (P < 0.05 and P < 0.01 compared to NC group by Kaplan-Meier’s statistics, respectively); all mice died by day 13 and 15, respectively (Figure 1B).


Allicin enhances host pro-inflammatory immune responses and protects against acute murine malaria infection.

Feng Y, Zhu X, Wang Q, Jiang Y, Shang H, Cui L, Cao Y - Malar. J. (2012)

Effects of allicin treatment on parasitaemia and survival of P. yoelii 17XL infected mice. Mice were treated with two doses of allicin (3 and 9 mg/kg) and PBS (control group) for successive three days after  P. yoelii 17 XL infection. Parasitaemia was calculated by counting the number of parasite-infected erythrocytes per 1,000 erythrocytes. Mortality was monitored daily. Results are presented as arithmetic mean of three mice per group ± the standard error of the mean (SEM). ##, significant difference (P < 0.001) compared to the control group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3472178&req=5

Figure 1: Effects of allicin treatment on parasitaemia and survival of P. yoelii 17XL infected mice. Mice were treated with two doses of allicin (3 and 9 mg/kg) and PBS (control group) for successive three days after P. yoelii 17 XL infection. Parasitaemia was calculated by counting the number of parasite-infected erythrocytes per 1,000 erythrocytes. Mortality was monitored daily. Results are presented as arithmetic mean of three mice per group ± the standard error of the mean (SEM). ##, significant difference (P < 0.001) compared to the control group.
Mentions: The P. yoelii 17XL strain is highly virulent to BALB/c mice and causes lethal infection. In the control group, parasitaemia rose sharply and reached a peak level (51.8%) on day 5 PI (Figure 1A) and all mice died by day 7 (Figure 1B). In contrast, three-day oral allicin treatments at two dosages significantly reduced the day 5 parasitaemias (27.1% and 32.6% for the 3 and 9 mg/kg groups, respectively). Further decline of the parasitaemia was noticed on day 7 PI in both allicin treatment groups (Figure 1A). Consistent with an earlier observation on the effect of allicin on Plasmodium berghei erythrocytic infection[30], allicin treatments at both dosages significantly extended the survival time of infected mice (P < 0.05 and P < 0.01 compared to NC group by Kaplan-Meier’s statistics, respectively); all mice died by day 13 and 15, respectively (Figure 1B).

Bottom Line: This effect is at least partially due to improved host immune responses.The absolute numbers of CD4+ T cells, DCs and macrophages were significantly higher in allicin-treated mice.In addition, allicin promoted the maturation of CD11c+ DCs, whereas it did not cause major changes in IL-4 and the level of anti-inflammatory cytokine IL-10.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Immunology, College of Basic Medical Sciences, China Medical University, Shenyang, Liaoning, China.

ABSTRACT

Background: During malaria infection, multiple pro-inflammatory mediators including IFN-γ, TNF and nitric oxide (NO) play a crucial role in the protection against the parasites. Modulation of host immunity is an important strategy to improve the outcome of malaria infection. Allicin is the major biologically active component of garlic and shows anti-microbial activity. Allicin is also active against protozoan parasites including Plasmodium, which is thought to be mediated by inhibiting cysteine proteases. In this study, the immunomodulatory activities of allicin were assessed during acute malaria infection using a rodent malaria model Plasmodium yoelii 17XL.

Methods: To determine whether allicin modulates host immune responses against malaria infection, mice were treated with allicin after infection with P. yoelii 17XL. Mortality was checked daily and parasitaemia was determined every other day. Pro-inflammatory mediators and IL-4 were quantified by ELISA, while NO level was determined by the Griess method. The populations of dendritic cells (DCs), macrophages, CD4+ T and regulatory T cells (Treg) were assessed by FACS.

Results: Allicin reduced parasitaemia and prolonged survival of the host in a dose-dependent manner. This effect is at least partially due to improved host immune responses. Results showed that allicin treatment enhanced the production of pro-inflammatory mediators such as IFN-γ, TNF, IL-12p70 and NO. The absolute numbers of CD4+ T cells, DCs and macrophages were significantly higher in allicin-treated mice. In addition, allicin promoted the maturation of CD11c+ DCs, whereas it did not cause major changes in IL-4 and the level of anti-inflammatory cytokine IL-10.

Conclusions: Allicin could partially protect host against P. yoelii 17XL through enhancement of the host innate and adaptive immune responses.

Show MeSH
Related in: MedlinePlus