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Dermatophytoses is a superficial fungal infection of tissues having keratin. The responsible fugus are dermatophytes. The infection is usually designated as ring worm or “tinea”. It is observed worldwide with higher prevalence in tropical countries and areas due to high rates of humidity, moisture and high sweating in summer. Recurrent dermatophytosis is a challenge for dermatologists in India and constituted 9.3% of all patients of dermatophytosis. The present study is conducted to reveal the prevalence of dermatophytosis in patients attended in the Maheshwari Hospital and Diagnostic Centre in Badaun. A survey was done for a period of one and half year. The samlples were obtained from Maheshwari Hospital and Diagnostic Centre, Badaun, Uttar Pradesh. A total of 300 patients were included in the study. Physical observation, KOH test, Microscopy and culture tests were performed for screening and confirmation of various fungal infections. Clinically the prevalence of dermatophytosis was 60% that was observed more in males. Patients with age group 16–30 and 31–40 years were more affected.

Cysteinyl leukotrienes (CysLTs), a group of inflammatory lipid mediators, are found elevated in obese-asthmatic patients. Leukotriene D4 (LTD4), a representative CysLT, is implicated in promoting lung inflammation and remodelling in allergic asthma, but its role in non-allergic asthma, especially in obese-asthmatic patients, is not known. Here, using primary human small airway epithelial cells (SAECs) we have investigated the mechanism of LTD4-induced inflammation and remodelling and assessed high proneness of obese mice to develop asthma upon challenge with allergen ovalbumin (OVA). Primary human small airway epithelial cells (SAECs) were stimulated with different concentrations of LTD4 for different time intervals and various inflammatory markers were measured through cytokine array, membrane-based ELISA and Western blotting. An air–liquid interface (ALI) model of SAECs was used to study the effects of LTD4-induced remodelling in SAECs using Western blotting, H&E staining and PAS staining. Further, OVA-based murine model was used to examine the propensity of high-fat diet (HFD)-fed obese mice to develop asthma symptoms by studying the infiltration of inflammatory cells (assessed by bronchioalveolar lavage (BAL) cytology) and airway remodelling (assessed by histopathology) upon allergen exposure. The human primary small airway epithelial cells (SAECs) treated with LTD4 showed significant alterations in the levels of inflammatory markers such as GM-CSF, TNF-α, IL-1β, EGF and eotaxin in dose- and time-dependent manner. Further, LTD4 enhanced the activation of inflammasomes as evidenced by increased levels of NALP3, cleaved caspase-1 and IL-1β. LTD4 also enhanced inflammation by increasing the expression of COX-2 in SAECs. The airway remodelling markers Vimentin and Muc5AC were found elevated in ALI culture of SAECs when stimulated with LTD4, as it also increased TGF-β levels and activation of Smad2/3 phosphorylation in SAECs. Last, sensitization and challenge of HFD-fed obese mice with OVA showed increased infiltration of inflammatory cells in BAL and enhanced levels of remodeling phenotypes like loss of cilia, mucus cell metaplasia and collagen deposition in mice lung tissues. The results suggest that LTD4 could induce inflammatory response in human airway epithelial cell by activating NALP3 inflammasome. LTD4 could further promote airway epithelial cells’ remodelling through TGF-β/smad2/3-mediated pathway. Our in vivo results suggested that obesity predisposed the OVA challenged mice to develop lung inflammation and remodelling akin to asthma-like phenotypes during obesity.

Airway epithelial cells arrayed in the inner lining of the airways of the lung are believed to be the major source for the development of malignancy of the lung. The advent of in vitro cell culture model made it easy to understand the molecular mechanism of carcinogenesis at a cellular level, where the airway epithelial cells are cultured on a 2D surface submerged in the culture media. However, this method of culturing airway epithelial cells does not reflect their true nature, and thus results obtained have their limitations. Further, they exhibit dissimilar morphology, transcriptome, and secretome when compared to the cells in vivo. Thus, the experimental data obtained from 2D culture models are inconclusive and, in most cases, could not be validated further in in vivo settings. These limitations can be addressed by culturing the airway epithelial cells on air-liquid interface (ALI), where they develop ciliated morphology similar to that of the lung. Experiments performed with this 3D model provide reliable data that are more realistic, and, in many cases, could replace the requirement of further in vivo validation. Here, we provide the detailed protocol of a 3D culture system called ALI culture for growing human-derived primary small airway epithelial cells to study the cellular and molecular changes associated with lung cancer.

Superparamagnetic iron oxide nanoparticles are much desired for various biomedical applications due to their biocompatible, biodegradable and superparamagnetic nature. In contrast to high-temperature synthesis methods, present study investigates the facile low-temperature co-precipitation process without inert atmosphere. For its efficient, homogenous, in core heating and environment friendly nature microwave energy at two powers of 180 and 450 W was used for synthesis and functionalisation of nanoparticles. It was found in the study, that microwave power plays a decisive role in controlling the size, coating and drug loading percentage of the particles. The synthesis process has been made more economic and simpler by the use of domestic oven, and serine coated particles with mean sizes around 6.8 and 10 nm, narrow size distribution (standard deviations of 1.4 and 1.6 nm), almost rectangular shape and magnetization values of approx. 48 and 42 emu/g were obtained at 180 and 450 W power, respectively. Particles were found to have properties such as near to zero remanence and coercivity, good crystallization and colloidal stability. The biocompatibility of the uncoated and serine coated particles was confirmed by the MTT assay on A 549 epithelial cells. Synthesized particles were found to have all the suitable properties for potential application in biomedical fields. Doxorubicin hydrochloride was loaded efficiently on both the synthesized particles, with loading efficiency obtained up to 6.8% wt/wt, for assessing their suitability as potential drug delivery agents.

Cysteinyl leukotrienes (CysLTs), a group of inflammatory lipid mediators, are found elevated in obese-asthmatic patients. Leukotriene DPrimary human small airway epithelial cells (SAECs) were stimulated with different concentrations of LTDThe human primary small airway epithelial cells (SAECs) treated with LTDThe results suggest that LTD

Background Cysteinyl leukotrienes (CysLTs), the potent lipid inflammatory mediators, are elevated in many pathological conditions and implicated in various inflammatory diseases including asthma, however their role in airway epithelial cells modulation is not clearly understood. We have investigated the effects of a CysLT, Leukotriene D4 (LTD4) on human airway epithelial cells, and assessed its role and mode of action in these cells. Methodology Human small airway epithelial cells (SAECs) and A549 cells were incubated with different concentrations of LTD4 for different time intervals. Subsequently trypan blue dye exclusion assay, MTT assay, Western blotting, RT-PCR and immunofluorescence experiments were performed to examine the effects of LTD4 on proliferation and related molecular changes in the airway epithelial cells. Results The treatment of human airway epithelial cells with LTD4 resulted in a significant increase in cell proliferation and modulation in the expression of receptors, CysLT1R and CysLT2R in SAECs as well as A549 cells. In both types of cells, LTD4 increased the expression levels of PCNA and c-myc, and trans-activated EGF receptor and increased the activation of ERK1/2. When treated along with epidermal growth factor (EGF), LTD4 showed a marginal additive effect in ERK1/2 and EGFR phosphorylation compared to LTD4 alone in both types of airway epithelial cells. Conclusion In conclusion, these results suggest that sustained presence of lipid inflammatory mediator LTD4 could induce human airway epithelial cell proliferation through ERK1/2 phosphorylation, either directly via CysLT1 receptor or by transactivating EGFR.

The cellular systems of living organisms are orchestrated with crucial events of constant production and removal of reactive oxygen species under physiological conditions. This plays an important biological role of maintenance of redox homeostasis and provides protection against oxidative stress-induced chronic and degenerative diseases. This chapter includes a detailed discussion on oxidative stress-induced inflammatory diseases such as asthma, cardiovascular diseases, diabetes, cancer and neurodegenerative diseases. Also, the modern approaches to studying oxidative stress-induced pathologies and key molecules that could act as therapeutic targets have been highlighted. The identification of oxidative stress as a common denominator to these diseases and the respective molecular targets that trigger these pathologies can potentially lead to novel approaches in disease prevention and health maintenance, especially via the use of nutraceuticals and/or phytochemicals. The paradoxical role of these nutraceuticals narrates the difficulties in using them clinically. Therefore, enhanced understanding of biochemical activities of nutraceuticals will enable them as better therapeutic options in oxidative stress-induced diseases.

Cysteinyl leukotrienes (CysLTs), the potent lipid inflammatory mediators, are elevated in many pathological conditions and implicated in various inflammatory diseases including asthma, however their role in airway epithelial cells modulation is not clearly understood. We have investigated the effects of a CysLT, Leukotriene DHuman small airway epithelial cells (SAECs) and A549 cells were incubated with different concentrations of LTDThe treatment of human airway epithelial cells with LTDIn conclusion, these results suggest that sustained presence of lipid inflammatory mediator LTD

Oxidative stress is a common denominator in many inflammatory diseases. A number of genetic and molecular factors are known to regulate oxidative stress by modulating cellular redox imbalance. These events lead to molecular and biochemical changes within the cells resulting in a myriad of biological phenomena including cell growth, initiation and progression of inflammation, programmed cell death, and cellular senescence. Reactive oxygen species (ROS) are well known to act as important secondary messengers which regulate gene expression through signal transduction pathways especially the MAP kinase and NF-κB pathway. Additionally, other molecular cascades are also regulated by oxidants. These molecular and genetic alterations lead to several changes such as genetic mutations, mitochondrial stress, and changes in NADH/NAD+ ratio that further augment and aggravate oxidative stress leading to health deterioration and disease development. Antioxidants, on the other hand, regulate molecular pathways and gene expression within cells as part of the cellular defense system by destroying ROS through enzymatic and nonenzymatic mechanisms. In the present chapter, we discuss the genetic and molecular mechanisms that regulate oxidative stress and play a crucial role in human health and diseases.