scholarly journals Unity of bowel-lung axis and the role of beneficial microbiota in anti-infectious protection

2021 ◽  
Vol 4 (4) ◽  
pp. 355-361
Author(s):  
T.E. Taranushenko ◽  

NIH Human Microbiome Project determined particular attention of the worldwide medical community to the study of the human microbiome and the assessment of the impact of symbiont microorganisms in the development of various (not only gastrointestinal) disorders. Potential interactions between the bowel and lungs (bowel-lung axis) via microbiota that allow for the possible involvement of microorganisms in the development of respiratory diseases are actively debated. This paper reviews studies on the pattern of interactions between bowel and lungs in infectious diseases associated with mucosal inflammation. The association between gut microbiota and the protective barrier of the respiratory tract based on known mechanisms and novel data derived from recent studies on SARS-CoV-2 is discussed. The relevance of beneficial bacteria (symbionts) in local and systemic immune responses, their disease-modifying and, eventually, therapeutic strategymodifying properties, the ability to be a resource of preventive medicine and an orchestrating tool for infections are addressed. Practitioners’ difficulties with probiotics in preventive and treatment schedules for various conditions are highlighted. Finally, the use of probiotics in children with respiratory infections and COVID-19 is uncovered. KEYWORDS: microbiota, microbiome, probiotics, children, mucosal immunity, Bifidobacterium. FOR CITATION: Taranushenko T.E. Unity of bowel-lung axis and the role of beneficial microbiota in anti-infectious protection. Russian Journal of Woman and Child Health. 2021;4(4):355–361 (in Russ.). DOI: 10.32364/2618-8430-2021-4-4-355-361.

2018 ◽  
Vol 154 (6) ◽  
pp. S-89
Author(s):  
Caiyun Ma ◽  
Cui Zhang ◽  
Wei Wu ◽  
Mingming Sun ◽  
Zhanju Liu

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Maike Willers ◽  
Dorothee Viemann

Abstract Colonization of the intestine with commensal bacteria is known to play a major role in the maintenance of human health. An altered gut microbiome is associated with various ensuing diseases including respiratory diseases. Here, we summarize current knowledge on the impact of the gut microbiota on airway immunity with a focus on consequences for the host defense against respiratory infections. Specific gut commensal microbiota compositions and functions are depicted that mediate protection against respiratory infections with bacterial and viral pathogens. Lastly, we highlight factors that have imprinting effects on the establishment of the gut microbiota early in life and are potentially relevant in the context of respiratory infections. Deepening our understanding of these relationships will allow to exploit the knowledge on how gut microbiome maturation needs to be modulated to ensure lifelong enhanced resistance towards respiratory infections.


2020 ◽  
Vol 8 (2) ◽  
pp. 197
Author(s):  
Shomeek Chowdhury ◽  
Stephen S. Fong

The impact of microorganisms on human health has long been acknowledged and studied, but recent advances in research methodologies have enabled a new systems-level perspective on the collections of microorganisms associated with humans, the human microbiome. Large-scale collaborative efforts such as the NIH Human Microbiome Project have sought to kick-start research on the human microbiome by providing foundational information on microbial composition based upon specific sites across the human body. Here, we focus on the four main anatomical sites of the human microbiome: gut, oral, skin, and vaginal, and provide information on site-specific background, experimental data, and computational modeling. Each of the site-specific microbiomes has unique organisms and phenomena associated with them; there are also high-level commonalities. By providing an overview of different human microbiome sites, we hope to provide a perspective where detailed, site-specific research is needed to understand causal phenomena that impact human health, but there is equally a need for more generalized methodology improvements that would benefit all human microbiome research.


2020 ◽  
Vol 8 (2) ◽  
pp. 173
Author(s):  
Liliana Simões-Silva ◽  
Ricardo Araujo ◽  
Manuel Pestana ◽  
Isabel Soares-Silva ◽  
Benedita Sampaio-Maia

Factors influencing the occurrence of peritoneal dialysis (PD)-related infections are still far from fully understood. Recent studies described the existence of specific microbiomes in body sites previously considered microbiome-free, unravelling new microbial pathways in the human body. In the present study, we analyzed the peritoneum of end-stage kidney disease (ESKD) patients to determine if they harbored a specific microbiome and if it is altered in patients on PD therapy. We conducted a cross-sectional study where the peritoneal microbiomes from ESKD patients with intact peritoneal cavities (ESKD non-PD, n = 11) and ESKD patients undergoing PD therapy (ESKD PD, n = 9) were analyzed with a 16S rRNA approach. Peritoneal tissue of ESKD patients contained characteristically low-abundance microbiomes dominated by Proteobacteria, Firmicutes, Actinobacteria, and Bacteroidetes. Patients undergoing PD therapy presented lower species richness, with dominance by the Pseudomonadaceae and Prevotelaceae families. This study provides the first characterization of the peritoneal microbiome in ESKD patients, bringing new insight to the human microbiome. Additionally, PD therapy may induce changes in this unique microbiome. The clinical relevance of these observations should be further explored to uncover the role of the peritoneal microbiome as a key element in the onset or aggravation of infection in ESKD patients, especially those undergoing PD.


Author(s):  
Michael P. Wakeman

The elderly are a growing proportion of the global population. They are more susceptible to non-communicable diseases and respiratory viral diseases like influenza and covid19, which may lead to increased levels of morbidity and mortality than those of a younger generation. It is also reported that co-morbidities, especially diabetes, hypertension and coronary heart disease contribute significantly to the prognosis with these types of infections. That the immune system operates in a less efficient way as an individual ages, is now well understood and likely contributes significantly to this situation. The role of certain micronutrients in maintaining a healthy immune system is well recognised and demonstrated to play an important role both in preventing and controlling infection. However, for a number of reasons many elderly individuals have a less than optimal intake of many of the micronutrients that support the immune system. This review examines the contributory roles an aging immune system, suboptimal intake of micronutrients, comorbidities and the impact of the intake of medications typically used to treat them can play in the outcome of viral respiratory infections. It identifies the need for supplementation, especially in the elderly to support the immune system.


Endocrinology ◽  
2020 ◽  
Vol 161 (11) ◽  
Author(s):  
Gabrielle P Huizinga ◽  
Benjamin H Singer ◽  
Kanakadurga Singer

Abstract The coronavirus disease 2019 (COVID-19) pandemic has forced us to consider the physiologic role of obesity in the response to infectious disease. There are significant disparities in morbidity and mortality by sex, weight, and diabetes status. Numerous endocrine changes might drive these varied responses to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, including hormone and immune mediators, hyperglycemia, leukocyte responses, cytokine secretion, and tissue dysfunction. Studies of patients with severe COVID-19 disease have revealed the importance of innate immune responses in driving immunopathology and tissue injury. In this review we will describe the impact of the metabolically induced inflammation (meta-inflammation) that characterizes obesity on innate immunity. We consider that obesity-driven dysregulation of innate immune responses may drive organ injury in the development of severe COVID-19 and impair viral clearance.


2016 ◽  
Vol 242 (2) ◽  
pp. 127-139 ◽  
Author(s):  
Javier Cabrera-Perez ◽  
Vladimir P Badovinac ◽  
Thomas S Griffith

Sepsis is a poorly understood syndrome of systemic inflammation responsible for hundreds of thousands of deaths every year. The integrity of the gut epithelium and competence of adaptive immune responses are notoriously compromised during sepsis, and the prevalent assumption in the scientific and medical community is that intestinal commensals have a detrimental role in the systemic inflammation and susceptibility to nosocomial infections seen in critically ill, septic patients. However, breakthroughs in the last decade provide strong credence to the idea that our mucosal microbiome plays an essential role in adaptive immunity, where a human host and its prokaryotic colonists seem to exist in a carefully negotiated armistice with compromises and benefits that go both ways. In this review, we re-examine the notion that intestinal contents are the driving force of critical illness. An overview of the interaction between the microbiome and the immune system is provided, with a special focus on the impact of commensals in priming and the careful balance between normal intestinal flora and pathogenic organisms residing in the gut microbiome. Based on the data in hand, we hypothesize that sepsis induces imbalances in microbial populations residing in the gut, along with compromises in epithelial integrity. As a result, normal antigen sampling becomes impaired, and proliferative cues are intermixed with inhibitory signals. This situates the microbiome, the gut, and its complex immune network of cells and bacteria, at the center of aberrant immune responses during and after sepsis.


2008 ◽  
Vol 83 (6) ◽  
pp. 2623-2631 ◽  
Author(s):  
Roberto Calcedo ◽  
Luk H. Vandenberghe ◽  
Soumitra Roy ◽  
Suryanarayan Somanathan ◽  
Lili Wang ◽  
...  

ABSTRACT Recent studies indicate that great apes and macaques chronically shed adenoviruses in the stool. Shedding of adenovirus in the stool of humans is less prevalent, although virus genomes persist in gut-associated lymphoid tissue in the majority of individual samples. Chimpanzees have high levels of broadly reactive neutralizing antibodies to adenoviruses in serum, with very low frequencies of adenovirus-specific T cells in peripheral blood. A similar situation exists in macaques; sampling of guts from macaques demonstrated adenovirus-specific T cells in lamina propria. Humans show intermediate levels of serum neutralizing antibodies, with adenovirus-specific T cells in peripheral blood of all individuals sampled and about 20% of samples from the gut, suggesting a potential role of T cells in better controlling virus replication in the gut. The overall structure of the E3 locus, which is involved in modulating the host's response to infection, is degenerate in humans compared to that in apes, which may contribute to diminished evasion of host immunity. The impact of adenovirus persistence and immune responses should be considered when using adenoviral vectors in gene therapy and genetic vaccines.


2020 ◽  
Vol 28 (02) ◽  
pp. 377-429
Author(s):  
GIDEON A. NGWA ◽  
WOLDEGEBRIEL A. WOLDEGERIMA ◽  
MIRANDA I. TEBOH-EWUNGKEM

A within-human-host malaria parasite model, integrating key variables that influence parasite evolution-progression-advancement, under innate and adaptive immune responses, is analyzed. The implicit role of immunity on the steady state parasite loads and parasitemia reproduction number ([Formula: see text]), a threshold parameter measuring the parasite’s annexing ability of healthy red blood cells (HRBCs), eventually rendering a human infectious to mosquitoes, is investigated. The impact of the type of recruitment function used to model HRBC growth is also investigated. The model steady states and [Formula: see text], both obtained as functions of immune system variables, are analyzed at snapshots of immune sizes. Model results indicate that the more the immune cells, innate and adaptive, the more efficient they are at inhibiting parasite development and progression; consequently, the less severe the malaria disease in a patient. Our analysis also illustrates the existence of a Hopf bifurcation leading to a limit cycle, observable only for the nonlinear recruitment functions, at reasonably large [Formula: see text].


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