Expression of resistin, CXCR3, IP-10, CCR5 and MIP-1α in obese patients with different severity of asthma

Asthma studies suggest that alteration in the inflammation pattern may be associated with the severity of asthma. The aim of this study was to compare in vitro the expression of chemokines, chemokine receptors and cytokine production from CD4+ T human lymphocytes of asthmatic, both obese and non-obese patients with different severity levels of asthma. Lymphocytes were labeled with monoclonal anti-human CXCR3/IP-10, MIP-1a/CCR5 antibodies and were analyzed by flow cytometry. Cell culture supernatants were used to measure production of interleukin IL-6 and resistin by ELISA. CXCR3/IP-10 expression increased in non-obese patients with mild persistent asthma (2.2%, p<0.05), moderate persistent asthma (3%, p<0.003) and severe persistent asthma (4%, p<0.004); this effect was stronger in obese patients with severe persistent asthma (35%, p<0.004). MIP-1 α / CCR5 increased in non-obese patients with intermittent asthma (0.65%, p<0.05) and severe asthma (1.4%, p<0.03); in obese patients, this expression was greater in intermittent asthma (8%, p<0.05) and severe persistent asthma (12%, p<0.04). Resistin production strongly increased in obese patients with intermittent (976 ng/ml) and severe persistent asthma (795 ng/ml). IL-6 increased in both lean and obese persons; however, the highest value was registered in the group of severe persistent obese asthmatics (992 pg/ml). Obesity per se increased the inflammatory profile of chemokines / cytokines secreted by cells of the blood, increasing the inflammatory status in asthmatic patients. Resistin showed characteristics of a pro-inflammatory cytokine mainly in severely obese asthmatics.

Chemokine Receptor CCR3 Expression in Malignant Cutaneous Tumors

BACKGROUND: Chemokines and their receptors are important players in tumorigenesis by facilitating tumor proliferation and metastasis. Little is known about the possible function of chemokine receptors in relation to the development and progression of malignant cutaneous tumors. OBJECTIVE: The aim of this study was to determine the chemokine receptor CCR3 expression pattern and the protein expression level in selected malignant cutaneous tumors. METHODS: Four types of cell lines (G361, A431, SK-MEL-2, SK-MEL-24) were analyzed, using Western blotting, for the expression of CCR3 protein. Immunohistochemical staining for CCR3 was done on 36 skin cancer tissue samples that included 16 squamous cell carcinomas (SCCs), 16 basal cell carcinomas (BCCs), 16 malignant melanomas (MMs) and 6 normal tissue samples. RESULTS: Western blot analysis showed that CCR3 protein was more expressed in the MM cell lines (G361, SK-MEL-2,SK-MEL-24) than that in the SCC cell line (A431), and the immunohistochemical analysis showed that CCR3 protein was overexpressed in MM and SCC, it was mildly expressed in BCC and it was hardly expressed in normal tissue. CONCLUSION: This study demonstrated via immunochemistry that CCR3 was more expressed in MM, followed by SCC and BCC. The existence of CCR3 protein may enhance the tumorigenic potential of malignant cutaneous tumors.

Effect of the monocyte locomotion inhibitory factor (MLIF) produced by E. histolityca on cytokines and chemokine receptors in T CD4+ lymphocytes

Entamoeba histolytica produces Monocyte Locomotion Inhibitory Factor (MLIF), which may contribute to the delayed inflammation observed in amoebic hepatic abscesses. Leukocytes are affected through the modulation of cytokine expression and/or production. We evaluated the effects of MLIF on the activation and production of intracellular cytokines in human CD4+ T lymphocytes by flow cytometry. Cells were stimulated for 24 h with PMA, MLIF, or PMA+MLIF. Cellular activation was measured using anti-CD69. Th1/Th2 production was studied by the expression of intracellular cytokines and cytokine/chemokine receptors. MLIF increased CD69 and induced the over-expression of the IL-l©¬, IFN-¥ã, IL-2, IL-4, and IL-10 intracellular cytokines; PMA+MLIF inhibited Th1 cytokine (IFN-¥ã) and increased Th2 cytokines (IL-4 and IL-10). The co-expression of the cytokine and chemokine receptors IFN-¥ã/CCR5 and IL-1©¬/CCR5 was inhibited by PMA+MLIF and Th2 co-expression was increased. MLIF effects varied depending on the conditions. MLIF alone activated the Th1 and Th2 cytokines and cytokine/receptor expression; however, PMA+MLIF increased the expression of Th2 but inhibited it in Th1.