Advanced Role of Neutrophils in Common Respiratory Diseases

Liu, Jinping; Pang, Zhiqiang; Wang, Guoqiang; Guan, Xuewa; Fang, Keyong; Wang, Ziyan; Wang, Fang

doi:10.1155/2017/6710278

Cited by 79 publications

(76 citation statements)

References 236 publications

(273 reference statements)

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“…Upregulation of neutrophil chemoattractors (LTB 4 , CXCL1, CXCL5, IL-8, and TNF-α) induces a massive migration of circulating neutrophils into the lung parenchyma ( 96 ). The transmigration of blood neutrophils occurs through adherence of the granulocytes to E-selectin of endothelial cells that is found to be upregulated in COPD ( 97 ).…”

Section: Alteration Of Airway Gene Expression and Immune Response In mentioning

confidence: 99%

The Interplay Between Immune Response and Bacterial Infection in COPD: Focus Upon Non-typeable Haemophilus influenzae

Jalalvand

Thegerström

et al. 2018

Front. Immunol.

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Chronic obstructive pulmonary disease (COPD) is a debilitating respiratory disease and one of the leading causes of morbidity and mortality worldwide. It is characterized by persistent respiratory symptoms and airflow limitation due to abnormalities in the lower airway following consistent exposure to noxious particles or gases. Acute exacerbations of COPD (AECOPD) are characterized by increased cough, purulent sputum production, and dyspnea. The AECOPD is mostly associated with infection caused by common cold viruses or bacteria, or co-infections. Chronic and persistent infection by non-typeable Haemophilus influenzae (NTHi), a Gram-negative coccobacillus, contributes to almost half of the infective exacerbations caused by bacteria. This is supported by reports that NTHi is commonly isolated in the sputum from COPD patients during exacerbations. Persistent colonization of NTHi in the lower airway requires a plethora of phenotypic adaptation and virulent mechanisms that are developed over time to cope with changing environmental pressures in the airway such as host immuno-inflammatory response. Chronic inhalation of noxious irritants in COPD causes a changed balance in the lung microbiome, abnormal inflammatory response, and an impaired airway immune system. These conditions significantly provide an opportunistic platform for NTHi colonization and infection resulting in a “vicious circle.” Episodes of large inflammation as the consequences of multiple interactions between airway immune cells and NTHi, accumulatively contribute to COPD exacerbations and may result in worsening of the clinical status. In this review, we discuss in detail the interplay and crosstalk between airway immune residents and NTHi, and their effect in AECOPD for better understanding of NTHi pathogenesis in COPD patients.

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Section: Alteration Of Airway Gene Expression and Immune Response In mentioning

confidence: 99%

The Interplay Between Immune Response and Bacterial Infection in COPD: Focus Upon Non-typeable Haemophilus influenzae

Jalalvand

Thegerström

et al. 2018

Front. Immunol.

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“…In particular, this review will focus on the shared role of the neutrophil in these diseases. While neutrophils are not the only cells that play a role in COPD, atherosclerosis and T2D, they are the most abundant immune cells found in lung secretions of patients diagnosed with COPD and their products have been shown to cause all facets of lung disease in animal and cell models (from chronic bronchitis to emphysema); correlating with disease severity and decline [19,20]. Recent advances in imaging technologies have also identified that neutrophils are present in the lipid core of human plaques and neutrophilia correlates with the number of rupture-prone lesions [21] and, although less studied, diabetic patients, rats and mice clearly demonstrate consistent defects of neutrophil chemotactic, phagocytic and microbicidal activities [22].…”

Section: Introductionmentioning

confidence: 99%

Shared mechanisms of multimorbidity in COPD, atherosclerosis and type-2 diabetes: the neutrophil as a potential inflammatory target

2020

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Multimorbidity is increasingly common and current healthcare strategies are not always aligned to treat this complex burden of disease. COPD, type-2 diabetes mellitus (T2D) and cardiovascular disease, especially atherosclerosis, occur more frequently together than expected, even when risk factors such as smoking, obesity, inactivity and poverty are considered. This supports the possibility of unifying mechanisms that contribute to the pathogenesis or progression of each condition.Neutrophilic inflammation is causally associated with COPD, and increasingly recognised in the pathogenesis of atherosclerosis and T2D, potentially forming an aetiological link between conditions. This link might reflect an overspill of inflammation from one affected organ into the systemic circulation, exposing all organs to an increased milieu of proinflammatory cytokines. Additionally, increasing evidence supports the involvement of other processes in chronic disease pathogenesis, such as cellular senescence or changes in cellular phenotypes.This review explores the current scientific evidence for inflammation, cellular ageing and cellular processes, such as reactive oxygen species production and phenotypic changes in the pathogenesis of COPD, T2D and atherosclerosis; highlighting common mechanisms shared across these diseases. We identify emerging therapeutic approaches that target these areas, but also where more work is still required to improve our understanding of the underlying cellular biology in a multimorbid disease setting.

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“…IL-6 can mediate both pro-inflammatory and anti-inflammatory functions [ 138 ]. An acute increase in IL-6 facilitates neutrophil recruitment to sites of tissue injury in order to induce acute inflammation [ 143 ]. However, IL-6 also activates STAT3 signaling which facilitates the reduction in neutrophils in acute inflammation [ 144 ].…”

Section: Deficiency In Cell Signaling Molecules As Determinants Ofmentioning

confidence: 99%

Susceptibility Factors in Chronic Lung Inflammatory Responses to Engineered Nanomaterials

You

Bonner

2020

IJMS

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Engineered nanomaterials (ENMs) are products of the emerging nanotechnology industry and many different types of ENMs have been shown to cause chronic inflammation in the lungs of rodents after inhalation exposure, suggesting a risk to human health. Due to the increasing demand and use of ENMs in a variety of products, a careful evaluation of the risks to human health is urgently needed. An assessment of the immunotoxicity of ENMs should consider susceptibility factors including sex, pre-existing diseases, deficiency of specific genes encoding proteins involved in the innate or adaptive immune response, and co-exposures to other chemicals. This review will address evidence from experimental animal models that highlights some important issues of susceptibility to chronic lung inflammation and systemic immune dysfunction after pulmonary exposure to ENMs.

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Advanced Role of Neutrophils in Common Respiratory Diseases

Cited by 79 publications

References 236 publications

The Interplay Between Immune Response and Bacterial Infection in COPD: Focus Upon Non-typeable Haemophilus influenzae

The Interplay Between Immune Response and Bacterial Infection in COPD: Focus Upon Non-typeable Haemophilus influenzae

Shared mechanisms of multimorbidity in COPD, atherosclerosis and type-2 diabetes: the neutrophil as a potential inflammatory target

Susceptibility Factors in Chronic Lung Inflammatory Responses to Engineered Nanomaterials

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