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Introduction: The COVID-19 pandemic in India has resulted in mass destruction in the form of second wave.Indian citizens and government were badly affected and were left constrained with basic medical facilities in treating the heavy load of patients. The possibility of reemergence of virulent strains of SARS-CoV-2 still exists., Area Covered: In this article, we tend to discuss why India is at high risk to be to be affected by the other waves and what strategies could be implemented to contain the viral spread. It provides these insights with reference to the gaps and the lessons learnt from the second wave along with the possible solutions to tackle these problems that were not effectively handled during the previous episodes of viral spread. We propose strategies for implementing effective vaccination programs, focus on speeding up different ways of diagnosis, management of essential hospital aids, prevention from vaccine escape mutant strains  and implementation of COVID-appropriate behavior in rural areas of India., Expert Opinion: This article has significance to the researchers and government officials in understanding the gaps that led to COVID-19 second wave in India and provides an opportunity to improve on certain areas for handling the future waves with more vigilance. Abbreviations: COVID-19 - Coronavirus disease 2019; SARS-COV-2 - severe acute respiratory syndrome - Coronavirus 2; δ - Delta variant; δ+ - Delta plus variant; WHO - World Health Organization; RT -PCR - Reverse transcription PCR; IFN-1 - Interferon 1; VOCs - Variants of concern; HCWs - healthcare workers.

Introduction: COVID-19 is a recent emerging pandemic whose prognosis is still unclear. Diagnostic tools are the main players that not only indicate a possible infection but can further restrict the transmission and can determine the extent to which disease progression would occur., Areas Covered: In this paper, we have performed a narrative and critical review on different technology-based diagnostic strategies such as molecular approaches including real-time reverse transcriptase PCR, serological testing through enzyme-linked immunosorbent assay, laboratory and point of care devices, radiology-based detection through computed tomography and chest X-ray, and viral cell cultures on Vero E6 cell lines are discussed in detail to address COVID-19. This review further provides an overview of emergency use authorized immunodiagnostic and molecular diagnostic kits and POC devices by FDA for timely and efficient conduction of diagnostic tests. The majority of the literature cited in this paper is collected from guidelines on protocols and other considerations on diagnostic strategies of COVID-19 issued by WHO, CDC, and FDA under emergency authorization., Expert Opinion: Such information holds importance to the health professionals in conducting error-free diagnostic tests and researches in producing better clinical strategies by addressing the limitations associated with the available methods.

Introduction: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, and irreversible fibrotic disease associated with respiratory failure. The disease remains idiopathic, but repeated alveolar epithelium injury, disruption of alveolar-capillary integrity, abnormal vascular repair, and pulmonary vascular remodeling are considered possible pathogenic mechanisms. Also, the development of comorbidities such as pulmonary hypertension (PH) could further impact disease outcome, quality of life and survival rates in IPF., Areas Covered: The current review provides a comprehensive literature survey of the mechanisms involved in the development and manifestations of IPF and their links to PH pathology. This review also provides the current understanding of molecular mechanisms that link the two pathologies and will specifically decipher the role of endothelial to mesenchymal transition (EndMT) along with the possible triggers of EndMT. The possibility of targeting EndMT as a therapeutic option in IPF is discussed., Expert Opinion: With a steady increase in prevalence and mortality, IPF is no longer considered a rare disease. Thus, it is of utmost importance and urgency that the underlying profibrotic pathways and mechanisms are fully understood, to enable the development of novel therapeutic strategies.

Introduction: Chronic obstructive pulmonary disease (COPD) is primarily an airway condition, which mainly affects cigarette smokers and presents with shortness of breath that is progressive and poorly reversible. In COPD research, there has been a long held belief that airway disease progression is due to inflammation. Although this may be true in the airway lumen with innate immunity activated by the effect of smoke or secondary to infection, the accurate picture of inflammatory cells in the airway wall, where the pathophysiological COPD remodeling occurs, is uncertain and debatable. Areas covered: The current review provides a comprehensive literature survey of the changes in the main inflammatory cells in human COPD patients and focuses on contrarian views that affect the prevailing dogma on inflammation. The review also delves into the role of oxidative stress and inflammasomes in modulating the immune response in COPD. Further, the effects of inflammation in affecting the epithelium, fibroblasts, and airway remodeling are discussed. Expert commentary: Inflammation as a driving force for airway wall damage and remodelling in early COPD is at the very least 'oversimplified' and is likely to be misleading. This has serious implications for rational thinking about the illness, including pathogenesis and designing therapy.

The authors established that cigarette smoke increases airway epithelial platelet activating factor receptor (PAFr) expression and that PAFr is markedly up-regulated in the lungs of chronic obstructive pulmonary disease (COPD) patients. Crucially, PAFr is used by the two key bacterial species involved in chronic infection and acute exacerbations in COPD, that is, Streptococcus pneumoniae and Haemophilus influenzae, as a receptor for lung epithelial colonization. The cognate adhesin of PAFr, phosphorylcholine (ChoP), in the cell wall of these bacterial species may be a key effector that underpins host colonization. In this review, the authors evaluate the respective roles of PAFr and ChoP in the natural history of COPD and discuss the potential of the airway epithelial PAFr-bacterial ChoP interaction as a selective anti-infective target in COPD therapeutics.

Current drug therapies for ulcerative colitis (UC) are not completely effective in managing moderate-to-severe UC and approximately 20% of patients with severe UC require surgical interventions. Heparins, polydisperse mixtures of non-anticoagulant and anticoagulant oligosaccharides, are widely used as anticoagulants. However, heparins are also reported to have anti-inflammatory properties. Unfractionated heparin was initially used in patients with UC for the treatment of rectal microthrombi. Surprisingly, it was found to be effective in reducing UC-associated symptoms. Since then, several pre-clinical and clinical studies have reported promising outcomes of heparins in UC. In contrast, some controlled clinical trials demonstrated no or only limited benefits, thus the potential of heparins for the treatment of UC remains uncertain. This review discusses potential mechanisms of action of heparins, as well as proposed reasons for their contradictory clinical effectiveness in the treatment of UC.

Chronic obstructive pulmonary disease (COPD) is a complex condition, frequently with a mix of airway and lung parenchymal damage. However, the earliest changes are in the small airways, where most of the airflow limitation occurs. The pathology of small airway damage seems to be wall fibrosis and obliteration, but the whole airway is involved in a 'field effect'. Our novel observations on active epithelial-mesenchymal transition (EMT) in the airways of smokers, particularly in those with COPD, are changing the understanding of this airway pathology and the aetiology of COPD. EMT involves a cascade of regulatory changes that destabilise the epithelium with a motile and mesenchymal epithelial cell phenotype emerging. One important manifestation of EMT activity involves up-regulation of specific key transcription factors (TFs), such as Smads, Twist, and β-catenin. Such TFs can be used as EMT biomarkers, in recognisable patterns reflecting the potential major drivers of the process; for example, TGFβ, Wnt, and integrin-linked kinase systems. Thus, understanding the relative changes in TF activity during EMT may provide rich information on the mechanisms driving this whole process, and how they may change over time and with therapy. We have sought to review the current literature on EMT and the relative expression of specific TF activity, to define the networks likely to be involved in a similar process in the airways of patients with smoking-related COPD.

Introduction: Approximately 300 million people worldwide are currently affected by asthma. Improvements in the understanding of the mechanisms involved in such inflammatory airway disorders has led to the recognition of new therapeutic approaches. Heparin, a widely used anticoagulant, has been shown to be beneficial in the management of asthma. It belongs to the family of highly sulphated polysaccharides referred to as glycosaminoglycans, containing a heterogeneous mixture of both anticoagulant and non-anticoagulant polysaccharides. Experimental findings have suggested that heparin has potential anti-asthmatic properties owing to the ability of its non-anticoagulant oligosaccharides to bind and modulate the activity of a wide range of biological molecules involved in the inflammatory process., Areas Covered: This review focuses on the potential mechanisms of action and clinical application of heparin as an anti-inflammatory agent for the management of asthma., Expert Opinion: Heparin may play a significant role in the management of asthma. However, these properties are often hindered by the presence of anticoagulant oligosaccharides, which possess a significant risk of bleeding. Therefore, its therapeutic potential must be explored using well-designed clinical studies that focus on identifying and isolating the anti-inflammatory oligosaccharides of heparin and further elucidating the structure and mechanisms of actions of these non-anticoagulant oligosaccharides.

The authors have reviewed the current literature on airway inflammation and remodeling in smoking-related chronic obstructive pulmonary disease (COPD). Detailed data on airway remodeling in COPD are especially sparse and how these changes lead to decline in lung function is not well understood. Small airway fibrosis and obliteration are likely to be the main contributors to physiological airway dysfunction and occur earlier than any subsequent development of emphysema. One potential mechanism contributing to small airway fibrosis/obliteration and change in extracellular matrix is epithelial-mesenchymal transition. When associated with angiogenesis (so-called epithelial-mesenchymal transition type 3) it may well also be the link with the development of cancer, which is closely associated with COPD, predominantly in large airways. The authors have focused on our recent publications in these areas. Further investigations teasing out these mechanisms will help improve our understanding of key airway disease processes in COPD, which may have major therapeutic implications.