The primary function of the lungs is gas exchange. Approximately 400 million years ago, the Earth’s atmosphere gained enough oxygen in the gas phase for the animals that emerged from the sea to breathe air. The first lungs were merely primitive air sacs with a few vessels in the walls that served as accessory organs of gas exchange to supplement the gills. Eons later, as animals grew accustomed to a solely terrestrial life, the lungs became highly compartmentalized to provide the vast air-blood surface necessary for O2 uptake and CO2 elimination, and a respiratory control system was developed to regulate breathing in accordance with metabolic demands and other needs. With the evolution and phylogenetic development, lungs were taking a variety of other specialized functions to maintain homeostasis, which we will call the non-respiratory functions of the lung and that often, and by mistake, are believed to have little or no connection with the replacement gas. In this review, we focus on the metabolic functions of the lung, perhaps the least known, and mainly, in the lipid metabolism and blood-adult lung vascular endothelium interaction. When these functions are altered, respiratory disorders or diseases appear, which are discussed concisely, emphasizing how they impact the most important function of the lungs: external respiration.

Inhaled bronchodilators are the mainstay of pharmacological treatment for stable chronic obstructive pulmonary disease (COPD), including β2-agonists and muscarinic antagonists. Tiotropium bromide, a long-acting antimuscarinic bronchodilator (LAMA), is a treatment choice for moderate-to-severe COPD; its efficacy and safety have been demonstrated in recent trials. Studies also point to a beneficial role of tiotropium in the treatment of difficult-to-control asthma and a potential function in the asthma-COPD overlap syndrome (ACOS). Combination of different bronchodilator molecules and addition of inhaled corticosteroids are viable therapeutic alternatives. A condensation of the latest trials and the rationale behind these therapies will be presented in this article.

SUMMARYHuman abdominal angiostrongyliasis is a zoonotic disease caused by ingestion of the L3 larvae of Angiostrongylus costaricensis. The human infection gives rise to a pathological condition characterized by acute abdominal pain, secondary to an inflammatory granulomatous reaction, marked eosinophilia and eosinophilic vasculitis. Most commonly this disease is limited to intestinal location, primary ileocecal, affecting the mesenteric arterial branches and intestinal walls. We present one of the few cases reported around the world with simultaneous involvement of the intestines and liver, including proved presence of nematodes inside the hepatic arteriole.

The human body makes free radicals all the time for useful purposes. The antioxidant levels and control systems recover any injury occurring. The enzymes that repair DNA damage by free radicals are especially important. Inhaled reactive oxidant species (ROS) and those endogenously formed by inflammatory cells constitute an increased intrapulmonary oxidative burden. In many diseases, the balance between oxidants and antioxidants (redox balance) is altered causing severe consequences. He proceeds to review the pathophysiological mechanisms by which free radicals generate various types of stress, such as oxidative stress, nitrative, carbonyl, inflammatory and stress of the endoplasmic reticulum. Later we discuss how these different types of stress affect respiratory functions in diseases such as chronic obstructive pulmonary disease (COPD), bronchial asthma (BA), bronchiectasis, and idiopathic pulmonary fibrosis (IPF). Finally, the role that various strategies to increase lung antioxidants and potentially beneficial effects of antioxidant therapy in the course of the disease are discussed.

Respiratory diseases are among the leading causes of morbidity and mortality in the world population. Our understanding of the molecular mechanisms leading to recognition of infectious pathogens and harmful endogenous signals by the innate immune system and the adaptive immune system has improved significantly in recent decades. There is increased evidence of the key role of the immune system with its pattern recognition receptors (PRRs) in infectious and non-infectious lung diseases. The PRRs are a family of sensors able to sense different microbial molecules as well as endogenous molecules which are released by the host tissue damage. The commitment of PRRs is a prerequisite for the initiation of immune and inflammatory response to infection and tissue injury that may be beneficial or harmful. The PRRs are germ-line encoded, evolutionarily conserved molecules and consist of Toll-like receptors, NOD-like receptors, RIG-I-like receptors, C-type lectin-like receptors and cytosolic DNA sensors. This review summarizes the prominent role of transmembrane and cytosolic PRRs in the pathogenesis of infectious and non-infectious lung diseases. The PRRs and their signals represent promising targets for prophylactic and therapeutic strategies in various lung diseases.