No abstract

Autophagy is increasingly identified as a central player in many cellular activities from cell proliferation to cell division, migration, and differentiation. However, it is also considered as a double-edged sword in cancer biology which either promotes oncogenesis/invasion or sensitizes the tumor cells to chemotherapy induced apoptosis. Recent investigations have provided direct evidence for regulation of cellular phenotype via autophagy pathway. One of the most important types of phenotype conversion is Epithelial-Mesenchymal-Transition (EMT), resulting in alteration of epithelial cell properties to a more mesenchymal form. In the current chapter, we provide a method which is established and being used in our laboratory for detection of autophagy and EMT in lung epithelial cells and show the involvement of autophagy in modulation of cellular phenotype.

Our findings indicate that in the DU group, the serum concentrations of IL-12 but not of IL-13 were influenced by bacterial CagA, independent of the VacA status, suggesting that high IL-12 levels may contribute to susceptibility to DU in CagA-positive individuals. These findings could possibly be considered to improve the predictive or prognostic values of inflammatory cytokines for DU, and also to design possible novel therapeutic approaches.

Lung cells are constantly exposed to various internal and external stressors that disrupt protein homeostasis. To cope with these stimuli, cells evoke a highly conserved adaptive mechanism called the unfolded protein response (UPR). UPR stressors can impose greater protein secretory demands on the endoplasmic reticulum (ER) resulting in the development, differentiation, and survival of these cell types to meet these increasing functional needs.Dysregulation of the UPR leads to the development of the disease. The UPR and ER stress are involved in several human conditions such as chronic inflammation, neurodegeneration, metabolic syndrome, and cancer. Further, potent and specific compounds that target the UPR pathway are under development as future therapies. The focus of this review is to thoroughly describe the effects of both internal and external stressors on the ER in asthma. Further, we discuss how the UPR signaling pathway is activated in the lungs to overcome cellular damage.We also present an overview of the pathogenic mechanisms with a brief focus on potential strategies for pharmacological interventions.

The IL-18 - 607C variant was associated with higher levels of serum IL-18 and an increased risk of DU. Moreover, our findings indicated that serum concentrations of IL-18 were influenced by CagA factor, irrespective of the VacA status, suggesting that high levels of IL-18 in CagA-positive subjects predisposes to susceptibility to DU.

No abstract

Our findings propose that TGFβ1 + 868 TT genotype and TT/GG diplotype may confer increased risk of brucellosis in the examined population.

Background: The present study aimed to evaluate the effects of different concentrations of CONPs on the OS status in kidney, lung, and serum of rats. Methods: Male Wistar Rats were treated intraperitoneally with 15, 30, and 60 mg/kg/day of CONPs. The biochemical parameters, including TAC, TTG, MDA, SOD, and CAT were assayed in serum, kidney, and lung tissues. Results: MDA decreased, but TTG and CAT increased in serum by the administration of CONPs at 15 mg/kg. In kidney homogenate obtained from the group treated with CONPs at 15 mg/kg, TAC, TTG, and CAT significantly increased compared to the control group. However, CONPs at 15, 30, and 60 mg/kg significantly decreased MDA level compared to the control group. In lung tissue, CONPs in doses of 15, 30 and 60 mg/kg significantly decreased CAT activity, TTG and TAC compared to the control group, while in kidney tissue, CONPs at the concentrations of 30 and 60 mg/kg significantly increased MDA compared to the control group. Conclusion: Our findings suggest that CONPs attenuate OS in the kidney and affect the serum levels of OSrelated markers but induce OS in the lung tissue in a dose-dependent manner.