Neutrophils and the inflammatory tissue microenvironment in the mucosa

Campbell, Eric L.; Kao, Daniel J.; Colgan, Sean P.

doi:10.1111/imr.12456

Cited by 20 publications

(18 citation statements)

References 108 publications

(216 reference statements)

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“…Examples of these niches include the bone marrow, placenta, the mucosal surface of the gastrointestinal tract and lymph nodes; at these sites, various aspects of immune cell maturation, development, tolerance and proliferation occur and give rise to immune homeostasis 1–3 (FIG. 1).…”

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confidence: 99%

“…However, hypoxia is a common feature in a number of physiological immunological niches, particularly at sites where cell proliferation and consequently metabolic demand are high. These niches can be considered to be subject to ‘physiological hypoxia’, where a normally structured tissue maintains controlled and consistent oxygen gradients, which regulate pathways that are important for controlling physiological processes 3,15,16 (BOX 1; FIG. 1).…”

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confidence: 99%

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Regulation of immunity and inflammation by hypoxia in immunological niches

2017

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Immunological niches are focal sites of immune activity that can have varying microenvironmental features. Hypoxia is a feature of physiological and pathological immunological niches. The impact of hypoxia on immunity and inflammation can vary depending on the microenvironment and immune processes occurring in a given niche. In physiological immunological niches, such as the bone marrow, lymphoid tissue, placenta and intestinal mucosa, physiological hypoxia controls innate and adaptive immunity by modulating immune cell proliferation, development and effector function, largely via transcriptional changes driven by hypoxia-inducible factor (HIF). By contrast, in pathological immunological niches, such as tumours and chronically inflamed, infected or ischaemic tissues, pathological hypoxia can drive tissue dysfunction and disease development through immune cell dysregulation. Here, we differentiate between the effects of physiological and pathological hypoxia on immune cells and the consequences for immunity and inflammation in different immunological niches. Furthermore, we discuss the possibility of targeting hypoxia-sensitive pathways in immune cells for the treatment of inflammatory disease.

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Regulation of immunity and inflammation by hypoxia in immunological niches

2017

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“…Further, the presence of the PMNs and subsequent metabolic requirements exhaust the microenvironmental oxygen to quantities nearing anoxia (39). This localized oxygen depletion leads to the stabilization, and thus the activation of the transcription factor, hypoxia-inducible factor-α (HIF1α), and activation of the HIF1α signaling pathway that resolves inflammation, and potentially provides a more tolerant local setting for the bacteria (40, 41). Under these oxygen-deprived conditions, HIF1α activation inhibits mTOR activity resulting in a potent anti-inflammatory microenvironment through the production and stimulation of T regulatory cells would regulate tissue damage (42, 43).…”

Section: Stage 1 Disease Resistancementioning

confidence: 99%

Immunometabolic Phenotype Alterations Associated with the Induction of Disease Tolerance and Persistent Asymptomatic Infection of Salmonella in the Chicken Intestine

Kogut

Arsenault

2017

Front. Immunol.

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The adaptation of Salmonella enterica to the eukaryotic host is a key process that enables the bacterium to survive in a hostile environment. Salmonella have evolved an intimate relationship with its host that extends to their cellular and molecular levels. Colonization, invasion, and replication of the bacteria in an appropriate host suggest that modification of host functions is central to pathogenesis. Intuitively, this subversion of the cell must be a complex process, since hosts are not inherently programmed to provide an environment conducive to pathogens. Hosts have evolved countermeasures to pathogen invasion, establishment, and replication through two types of defenses: resistance and tolerance. Resistance functions to control pathogen invasion and reduce or eliminate the invading pathogen. Research has primarily concentrated on resistance mechanisms that are mediated by the immune system. On the other hand, tolerance is mediated by different mechanisms that limit the damage caused by a pathogen’s growth without affecting or reducing pathogen numbers or loads. The mechanisms of tolerance appear to be separated into those that protect host tissues from the virulence factors of a pathogen and those that limit or reduce the damage caused by the host immune and inflammatory responses to the pathogen. Some pathogens, such as Salmonella, have evolved the capacity to survive the initial robust immune response and persist. The persistent phase of a Salmonella infection in the avian host usually involves a complex balance of protective immunity and immunopathology. Salmonella is able to stay in the avian ceca for months without triggering clinical signs. Chronic colonization of the intestinal tract is an important aspect of persistent Salmonella infection because it results in a silent propagation of bacteria in poultry stocks due to the impossibility to isolate contaminated animals. Data from our lab promote the hypothesis that Salmonella have evolved a unique survival strategy in poultry that minimizes host defenses (disease resistance) during the initial infection and then exploits and/or induces a dramatic immunometabolic reprogramming in the cecum that alters the host defense to disease tolerance. Unfortunately, this disease tolerance results in the ongoing human food safety dilemma.

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“…O que a princípio é paradoxal uma vez que estímulos lesivos superficiais já estão sendo captados e estimulam o processo migratório. 11,12 Analisando-se as mucosas das lâminas histológicas, foi possível observar a presença de células caliciformes naquelas que apresentavam metaplasia intestinal (MI). A patogênese da MI pode ser explicada por uma combinação de aspectos genéticos do H. pylori e do hospedeiro, associada a fatores ambientais, sendo o H. pylori o principal causador, sobretudo os organismos que expressam as proteínas CagA e OipA.…”

Section: Introductionunclassified