Recent studies have indicated that the interleukin-12/interferon-g (IFN-g) axis is important in mycobacterial infection susceptibility. Using an intronic (CA) n polymorphic microsatellite marker within the IFN-g receptor-1 (IFNGR1) gene, we have compared the allelic frequencies of this marker in hospitalized tuberculosis patients (n ¼ 120) with that of controls (n ¼ 87) from Rijeka, Croatia. We identified 13 (CA) n alleles in the tuberculosis patients, whereas only 10 were found in the controls. A significant difference between one allelic marker and the control group was observed (P ¼ 0.02, 95% confidence interval 0.14-0.94), suggesting a possible protective association. In contrast, several other allelic markers showed a trend towards association with the disease. We also found a trend towards an increased frequency in homozygosity of one allelic marker in patients (11.7%) as compared with controls (4.6%). We conclude that there is no evidence for disease association of the IFNGR1 gene marker in Mendeliantype (single-allele) inheritance. However, our results also suggest that unidentified allelic variations in the IFNGR1 gene might elevate or decrease the risk in this ethnic population, as a part of the multigenic predisposition to tuberculosis.

Genetic susceptibility to tuberculosis includes several unknown yet different loci each contributing to a small extent. Intronic polymorphisms within the interferon-g (IFN-g) gene IFNG Tþ874A and IFNG Gþ2109A correlate with the IFN-g production in vitro, and the frequency of potential high IFN-g producers was previously reported by others to be lower in patients than in controls from Sicily. The aim of this study was to determine whether there is an association between polymorphisms in the IFN-g gene and predisposition to tuberculosis. We analysed two IFNG SNPs (Tþ874A and Gþ2109A) in patients (n ¼ 253) hospitalized in Rijeka (Croatia) and controls (n ¼ 519) from the same area. Onefifth of the controls were healthy contacts of the diseased, and the rest were blood donors. IFNG alleles, their predicted haplotypes or genotypes were not associated with disease susceptibility. Thus, we could not reproduce results from Sicilian case-control study. However, T/Tþ874 (possible high IFN-g producer) and þ874A/A (putative low producer) genotypes were associated with microscopically positive-negative forms of disease. Haplotypes (Tþ874A and Gþ2109A) based on a prediction by software PHASE and subsequent genotype analysis corroborated these findings. Patients had significantly higher frequency of genotypes without T at þ874 (AA/AA; AA/AG and AG/AG) in microscopyor bacterial culture-positive groups compared with their negative counterparts. These data suggest an association with disease severity rather than susceptibility to tuberculosis in Croatian Caucasian population.

Girls who experienced early menarche are significantly more often overweight/obese. Overweight/obesity may be considered as one of the predictors for the early occurrence of menarche.

Lung cancer is one of the most common malignant diseases and is amongst the leading causes of death. Cell-mediated immune response and cytokines could play an important role in antitumour immunity. The aim of the study was to evaluate the cytokines', tumour necrosis factor-a (TNF-a), interleukin-1b (IL-1b) and IL-6, releasing capacity in patients with lung carcinoma and benign lung disease. A group of 41 patients were tested for the production of TNF-a, IL-1b and IL-6 in bronchoalveolar lavage (BAL) and blood. The levels of cytokines in the lung cancer patients were: (1) in BAL ± IL-6, 173 AE 85 pg/ml; TNF-a, 170 AE 116 pg/ml; and IL-1b, 473 AE 440 pg/ml; (2) in the blood ± IL-6, 197 AE 53 pg/ml; TNF-a, 311 AE 202 pg/ml; and IL-1b, 915 AE 239 pg/ml. Alveolar macrophages of the patients with a lung cancer secreted significantly more cytokines, IL-6 (P 0.0004) and IL-1b (P 0.0047), than alveolar macrophages of the patients with a nonmalignant lung cancer. However, significantly lower levels of cytokine production by the BAL cells were found in patients with small cell lung cancer. This production decreased further in phase IV of nonsmall cell lung cancer.