We studied the relationship of serum immunoglobulin-E (Ig-E) and interleukin-4 (IL-4) concentrations, eosinophil counts, and frequency of respiratory illness with passive smoking in 70 randomly selected children of smoking parents. Fifty randomly selected age-matched children of non-smoking parents served as controls. Children of smoking parents had higher frequency of respiratory illnesses per year (P < 0.01), significantly higher total leucocytic and eosinophil counts, higher percentage of eosinophils (P < 0.01), and higher serum IgE and IL-4 concentrations (P < 0.05) compared to the control group. Serum IgE level was correlated positively with the average number of smoked cigarettes/day, number of siblings, and total leucocytic count. Interleukin-4 concentrations were significantly correlated with the number of smoked cigarettes and IgE levels. Although IgE levels were higher in children of smoking parents (587 +/- 359 IU/ml) compared to controls (189 +/- 21 IU/ml), they did not differ significantly between children with and those without frequent respiratory illness (605 +/- 365 and 557 +/- 354 IU/ml, respectively). Interleukin-4 concentrations were significantly higher in children of smoking parents with frequent respiratory illness (1.8 +/- 0.5 pg/ml) v. those without frequent respiratory illness (1.3 +/- 0.45 pg/ml). Multiple logistic regression analysis revealed that the overall positivity of the risk factors predisposing to respiratory diseases in the study children was 79 percent, and the highest odds ratio was that for IL-4 (OR = 5.15). In conclusion, there is a significant increase in IL-4 and Ig-E concentrations, high eosinophil count and frequent respiratory symptoms in children of smoking parents. It remains that the current state of knowledge on health risks associated with passive smoking warrants that strong preventive action be promoted.

Breast cancer is the commonest malignancy of women in many parts of the world and comprises 18% of all female cancers. There is one million new cases in the world each year. Neopterin which is a pteridine produced by activation of monocytes by IFN-γ may be used as a marker of immune system activation. The biological function of neopterin is still largely unknown and certain pathophysiologic roles have only recently been elucidated. Therefore, the aim of this work was to investigate the role of neopterin in females with primary and metastatic breast cancer. The obtained results were correlated with different clinicopathological data of those patients. The study population included females with primary and metastatic breast cancer as well as healthy age matched females were taken as a control group. Peripheral blood mononuclear cells were separated from each subject under study by Ficoll-Hypaque density gradient centrifugation technique. The isolated cells were cultured with and without PHA and neopterin levels were measured in serum and culture supernatants by ELISA technique. The results showed that neopterin levels were lowest in serum, followed by culture supernatants without PHA and highest in culture supernatants with PHA in each studied group. The mean neopterin values in serum and culture supernatants with PHA of metastatic breast cancer patients were significantly higher than in the primary breast cancer patients and the control group. Our results also indicated that neopterin levels positively correlated with the tumor grade, tumor stage and the presence of metastasis. From all mentioned data it is clear that, measurement of neopterin either in serum or in culture supernatants with or without PHA can give an indication about immunological status of breast cancer patients' response to therapy and early detection of metastasis. It gives an important and valuable prognostic information before surgical intervention is performed.

Targeting toll-like receptors (TLRs), via TLR agonists, has been implicated in the regulation of immunometabolism. B-chronic lymphocytic leukemia (B-CLL) represents a suitable model for B-cell derived malignancies with shifted metabolic adaptations. Several signaling pathways have been found to be critical in metabolic reprogramming of CLL, including mechanistic target of rapamycin- hypoxia inducible factor-1α (mTOR- HIF-1α) pathway, the main metabolic regulator of glycolysis. Here, we investigated the effect of TLR7/8 agonist (Resiquimod) on the expression of mTOR and HIF-1α in patients with CLL. B cells were purified using Rosettesep Human B cell Enrichment Cocktail (Stem cell Technologies, Vancouver, BC, Canada#15,024) from peripheral venous blood of CLL patients (n = 20) and healthy individuals (n = 15). Isolated B cells were then cultured in both presence and absence of Resiquimod. Gene expression of mTOR and HIF-1α were assessed using qRT-PCR. Resiquimod significantly decreased mTOR and HIF-1α gene expression in both CLL (p < 0.001and p < 0.001, respectively) and Normal B cells (p = 0.004 and p = 0.001, respectively). Resiquimod may reprogram immunometabolism of malignant B-CLL cells via down-regulation of key glycolytic metabolic actors, mTOR and HIF-1α genes. Accordingly, Resiquimod may be an adjuvant as a therapeutic tool for CLL, which needs to be studied further.

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