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Pulmonary – Treatable traits
Published in Vibeke Backer, Peter G. Gibson, Ian D. Pavord, The Asthmas, 2023
Vibeke Backer, Peter G. Gibson, Ian D. Pavord
One difficulty in this area is that infection might have different effects at different stages in the development of airway disease. For example the ‘hygiene hypothesis’ suggests that exposure to microbial infections during early childhood protects against subsequent development of atopy and asthma. There is also a view that exposure to microbial infection during early childhood provokes the development of atopy and asthma and that the composition of the airway microbiome is important in the development of atopy and asthma. In patients with established airway disease, the increased risk of infections may reflect the negative effects of inflammation on airway architecture and biological barriers and more fundamental immune dysfunction beginning even before the clinical onset of asthma.
What's Causing My Gut Symptoms?
Published in Melissa G. Hunt, Aaron T. Beck, Reclaim Your Life From IBS, 2022
Melissa G. Hunt, Aaron T. Beck
But even more important for our purposes are the other unintended consequences of too much sterilization of our environment. First, those of us who live in the industrialized world are ending up with dumb immune systems. There is considerable evidence for the “hygiene hypothesis” that explains the dramatic rise in the incidence of a variety of autoimmune disorders in the developed world. It turns out that exposure to a wide range of microorganisms before age 5 is crucial to the development of the immune system. Parents of young children in daycare may bemoan the many sniffles, coughs, and runny noses their kids come home with. But they should take heart in knowing that their kids are much less likely to develop asthma or serious allergies by the time they’re 15 than kids who stayed home until they started kindergarten. When the immune system doesn’t get to learn who the bad guys are and how to fight them, it grows up not being able to distinguish the bad guys from the good guys, or even the bad guys from the self. This has led to a dramatic rise in autoimmune disorders, including allergies, asthma, lupus, rheumatoid arthritis, and inflammatory bowel diseases in the developed world. As one gastroenterologist I work with put it, “There’s a thin line between dying of cholera and developing Crohn’s.”
Immunology of Allergic Diseases
Published in Pudupakkam K Vedanthan, Harold S Nelson, Shripad N Agashe, PA Mahesh, Rohit Katial, Textbook of Allergy for the Clinician, 2021
Finally, the distinguished work of Hill et al in murine models shed light on the interrelationship of microbiota, hygiene hypothesis and emergence of asthma phenotype (Fig. 2.3). The microbiota inhabiting the normal, healthy colonic mucosa is predominantly gram negative and shed endotoxin as part of the spectrum of PAMPs. These PAMPS bind to TLR4 and in a MYD 88 dependent fashion activate the luminal B cells to preferentially produce IgA and IgG antibodies and thus maintain the integrity of the mucosal immunity. On the other hand, absence of MyD88 dependent-microbial stimulation, results in IgE production by B cells, expansion of basophils from the bone marrow and increased susceptibility to allergic disease (Hill et al. 2012). It remains to be studied if respiratory microbiota can similarly abrogate TH2 responses in the lung. TLR 9 activation by CpG oligodeoxynucleotides has been shown to inhibit IgE class switching by B cells and possibly mitigate airway hyper responsiveness in humans (Creticos et al. 2006, Pascal et al. 2018). CpG motifs are considered pathogen-associated molecular patterns (PAMPs) due to their abundance in microbial genomes but their infrequency in vertebrate genomes. The link between the hygiene hypothesis and susceptibility to allergic diseases, may be a reflection of multiple environmental hits to the microbiota, including antibiotics, infection and diet changes, paired with the possible genetic defects in the human host that prevent appropriate recovery of the microbiota after disruption.
Allergen immunotherapy: progress and future outlook
Published in Expert Review of Clinical Immunology, 2023
Lara Šošić, Marta Paolucci, Stephan Flory, Fadi Jebbawi, Thomas M. Kündig, Pål Johansen
Changes are environmental factors that have been seen as an explanation to the rise of allergic diseases in the last decades, especially pollutants [22] and epithelial-barrier damaging agents [2]. Environmental factors that may damage the epithelial barriers of skin and mucosa are enzymes, food surfactants, and emulsifiers in our food, detergents in cleaning agents, cigarette smoke, traffic exhaust, and microplastics [2]. The hygiene hypothesis, proposed as early as in 1989 [23], suggested the increase in allergies to be due to a lack of a TH1-immunity-triggering microorganisms early in childhood, leading to a heightened TH2-immunity and thus marking the beginning of the atopic march. Today, the hygiene hypothesis remains to be a prominent theory, with additional knowledge indicating a more complex mechanism and imbalance in the development of the early immune system leading to a tendency to develop sensitization in the first years of life [24]. Additionally, the role of the increased rates of cesarean delivery, the increased use of antibiotics early in life, westernized diet, and obesity, as well as other factors that change the composition of our microbiome, are being discussed as reasons for the rise of allergic diseases [25,26].
Early-life exposure to antibiotics and subsequent development of atopic dermatitis
Published in Expert Review of Clinical Pharmacology, 2022
Anna Cantarutti, Claudio Barbiellini Amidei, Andrea Stella Bonaugurio, Paola Rescigno, Cristina Canova
The mechanisms underlying the development of AD are largely due to an inflammation promoted by T-helper type 2 (Th2) cells, evidence suggests several different pathways may be involved. The hygiene hypothesis provides a possible explanation for the increased risk of developing allergic diseases that may be associated with a reduced microbial exposure as a result of very hygienic conditions in early life that may cause an imbalance in the antigenic exposures for the immune system, that may increase the risk of developing allergic diseases [3]. Early-life exposure to antibiotics seems to be associated with a disrupted maturation of the intestinal microbiome, leading to a condition defined as dysbiosis, that could predispose to the development of several immune-mediated conditions, including atopic dermatitis [4].
Association between Helicobacter pylori and risk of childhood asthma: a meta-analysis of 18 observational studies
Published in Journal of Asthma, 2022
Yuxia Chen, Xue Zhan, Donghai Wang
The ‘hygiene hypothesis’ postulates that the recent rise in the incidence of allergic disease is attributable to reduced exposure to certain microbes and infections during childhood; this view has gained widespread acceptance (4). The hygiene hypothesis of asthma signifies a shift from a Th1 response to a Th2 response; this is the main explanation for the increased prevalence of asthma in western countries, whereby improved hygiene reduces environmental stimulus of the Th1 response (5). Helicobacter pylori (H. pylori), a gram-negative bacterium that naturally colonizes the gastric mucosa, is usually acquired in early childhood; the bacterium often causes a chronic form of gastritis that remains mostly asymptomatic (6). Infection with H. pylori induces a stronger Th1 cellular immune response, which may counterbalance the pro-allergic Th2 response (7,8). Thus, we speculate that H. pylori plays a role in modulating the risk of childhood asthma.