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AIMTo assess the levels of different immune modulators in patients with hepatocellular carcinoma (HCC), in relation to other hepatic diseases.METHODSEighty-eight patients were included in the current study and represented patients with HCC (20), liver cirrhosis (28) and chronic hepatitis (CH; 25), and normal controls (NC; 15). Peripheral blood was isolated for immunophenotyping of active myeloid dendritic cells (mDCs; CD1c and CD40), mature inactive myeloid cells (CD1c and HLA), active plasmacytoid cells (pDCs; CD303 and CD40), mature inactive pDCs (CD30 and HLA), active natural killer (NK) cells (CD56 and CD161), active NK cells (CD56 and CD314) and inactive NK cells (CD56 and CD158) was done by flow cytometry. Serum levels of interleukin (IL)-2, IL-10, IL-12, IL-1β, interferon (IFN)-α, IFN-γ and tumor necrosis factor (TNF)-αR2 were assessed by ELISA.RESULTSActive mDCs (CD1C+/CD40+) and inactive mDCs (CD1c+/HLA+) were significantly decreased in HCC patients in relation to NC (P < 0.001). CD40+ expression on active pDCs was decreased in HCC patients (P < 0.001), and its level was not significantly changed among other groups. Inactive pDCs (CD303+/HLA+), inactive NKs (CD56+/CD158+) and active NKs (CD56+/CD161+) were not statistically changed among the four groups studied; however, the latter was increased in CH (P < 0.05). NKG2D was statistically decreased in HCC, CH and cirrhosis (P < 0.001), and it was not expressed in 63% (12/20) of HCC patients. There was significant decrease of IL-2, IFN-α and IFN-γ (P < 0.001), and a significant increase in IL-10, IL-1β, and TNF-αR2 (P <0.01, P < 0.001 and P < 0.001; respectively) in HCC patients. There was inverted correlation between IL-12 and IL-1β in HCC (r = -0.565, P < 0.01), with a strong correlation between pDCs (CD303+/CD40+) and NKs (CD56+/CD161+; r = 0.512, P < 0.05) as well as inactive mDCs (CD1c+/HLA+) and inactive NK cells (CD56+/CD158+; r = 0.945, P < 0.001).CONCLUSIONNKG2D, CD40, IL-2 and IL-10 are important modulators in the development and progression of HCC.

The third-stage (L3) larvae of Anisakis are the etiological agents of human anisakiasis caused by consumption of raw or undercooked seafood infected with anisakid nematodes. Infection with these worms is associated with abdominal pain, nausea, and diarrhea and can lead to massive infiltration of eosinophils and the formation of granulomas in the gastrointestinal tract if the larvae are not removed. Food allergy affects populations worldwide, and despite several reports on the presence of the potentially zoonotic nematodes among edible fishes in Egypt, there are few immunological and molecular studies investigating the epidemiology of these parasites. Anisakidosis, a human infection with nematodes of the family Anisakidae, is caused most commonly by Anisakis spp. In the present study, seventy specimens of the European seabass Dicentrarchus labrax commercialized in Alexandria city along the Mediterranean Sea were acquired during the period from July to December, 2015. Fish were necropsied and dissected to investigate the presence of nematode larvae. Thirty fish (42.9%) of the total were parasitized by nematode larvae which were morphologically identified as Anisakis spp. Type II (L3) according to light and scanning electron microscopy. The pathogenic potential of oral inoculation of fresh, frozen, and thermally treated larvae into Wistar rats was elucidated by histological examination of their thymus and spleen. Results obtained indicated that neither cooling nor freezing of the parasite could destroy their allergenic capacity. So, it is important to create a wider awareness of this potential risk to human health. It is becoming increasingly likely that the impact of Anisakis spp. on human health has been underestimated, and it is perhaps time to consider more sweeping measures than those currently enforced to protect the public health.

Objectives This study aimed to assess the immunomodulatory effect of curcumin on innate and adaptive immune responses, as well as its inhibitory power on hyperglycemia in streptozotocin (STZ)-induced diabetic CD1 mice. Material and methods Mice were divided into six groups as follows: normal control mice (I), mice were intraperitoneally (i.p.) injected with either citrate (II), DEMSO (III), or curcumin (170 mg/kg, 3 times/week, for 28 days) (IV), as well as a single intraperitoneal injection of STZ (160 mg/kg) (V) and STZ mice treated with curcumin (VI). The anti-diabetic effect was assessed by estimation of the blood glucose concentration on days 3, 10, 17, 24, and 31. Differential count of white blood cells and the levels of cytokines were also measured at all previous time points. Pancreatic islets were examined for histopathological changes, and the immunohistochemical analysis for insulin and phosphorylated-nuclear factor-kappa B (phospho-NF-κB) was done at the end of the study. Results After curcumin administration, hyperglycemia was improved compared to diabetic mice; however, glucose concentration remains above the normal level. Treatment with curcumin selectively increased the count of lymphocytes and monocytes but decreased the granulocyte count in STZ diabetic mice. Diabetic mice treated with curcumin showed lower levels of interferon (IFN)-γ, interleukin (IL)-6, and IL-1β, as well as a higher level of IL-2 than in diabetic mice. Histopathological alterations that accompanied diabetes induction were ameliorated after curcumin administration. The pancreatic islets of treated diabetic mice displayed a decline in the immunostaining positivity of phospho-NF-κB compared to diabetic mice. Conclusion These results suggest that curcumin has anti-diabetic properties as it can improve the damage caused to the pancreatic β cells by its preferential immunomodulatory action on T helper1-related cytokines, as well as the immunosuppressive activity on proinflammatory cytokines.

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