Expression of Toll-like Receptor 2 and 4 in Peripheral Blood Neutrophil Cells from Patients with Chronic Obstructive Pulmonary Disease

Tripathi, Prashant Mani; Kant, Surya; Yadav, Ravi; Kushwaha, Ramesh Kumar; Prakash, Ved; Rizvi, Syed Husain Mustafa; Parveen, Arshiya; Mahdi, Abbas Ali; Ahmad, Iqbal

doi:10.5001/omj.2017.92

Cited by 9 publications

(8 citation statements)

References 35 publications

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“…The intrinsically reduced expression of TLRs in COPD patients may also contribute to the impaired pulmonary immune response thus facilitating NTHi persistent colonization. Expression of TLR2 or TLR4 are found to be lower on sputum neutrophils, alveolar macrophages, nasal epithelium, and T cells in COPD patients despite high concentrations of IL-8 and MMP-9 ( 295 – 298 ).…”

Section: Impaired Immunity In Copd In Response To Nthi Infection—currmentioning

confidence: 98%

“…Inversely, peripheral blood neutrophils isolated from COPD patients have increased expression of TLR2, TLR4, and NLRP3 ( 298 , 300 ). Nevertheless, the increased TLRs expression might not improve the microbicidal ability of COPD peripheral neutrophils probably due to the inaccurate responses to cytokines ( 179 ).…”

Section: Impaired Immunity In Copd In Response To Nthi Infection—currmentioning

confidence: 99%

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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: Impaired Immunity In Copd In Response To Nthi Infection—currmentioning

confidence: 98%

Section: Impaired Immunity In Copd In Response To Nthi Infection—currmentioning

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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“…A number of researchers have demonstrated that the effect of LPS on neutrophils from smokers with COPD results in an increase in TLR2/ TLR4 expression and a subsequent enhancement of the synthesis of IL-8 and matrix metalloproteinase-9 (MMP-9). 10,44 It has been revealed that TLR9 can also contribute to the cigarette smoke-mediated neutrophilic response by providing IL-8 secretion from circulating neutrophils. 4 Apparently, an enhanced blood neutrophilic response in COPD can be triggered by both bacterial or viral infection and cigarette smoke.…”

Section: Tlr2 and Tlr4 In The Development Of Copd Exacerbationmentioning

confidence: 99%

<p>The Role of Toll-Like Receptors 2 and 4 in the Pathogenesis of Chronic Obstructive Pulmonary Disease</p>

Sidletskaya

Виткина

Denisenko

2020

COPD

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Currently, chronic obstructive pulmonary disease (COPD) is one of the leading causes of morbidity and mortality worldwide. The determination of immune mechanisms of inflammation in the disease presents an important challenge for fundamental medical research. According to modern views, Toll-like receptors (TLRs), among which TLR2 and TLR4 play a key role, are one of the essential components of inflammatory process in COPD. This review focuses on following aspects: the role of TLR2 and TLR4 in the initiation of inflammatory process in COPD; the mechanisms of influence of various exogenous factors (cigarette smoke, suspended particulate matter, and bacteria) on the expression of TLR2 and TLR4; the contribution of these TLRs to the T-helper (Th) immune response development in COPD, in particular to the Th17 immune response, which contributes to the progression of the disease and therapeutic implications of TLR2 and TLR4 in COPD.

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“…Neutrophils are the dominant circulating leukocyte. Bacterial extract, LPS, induces peripheral circulating neutrophils from COPD patients to secrete higher amounts of IL-8/CXCL8 ( 20 , 21 ) as well as matrix metalloproteinase 9 ( 21 ). Moreover, several studies suggested that neutrophils from COPD patients display increased migration toward inflammatory stimuli ( 22 , 23 ).…”

Section: Innate Immune Systemmentioning

confidence: 99%

Roles of Myeloid and Lymphoid Cells in the Pathogenesis of Chronic Obstructive Pulmonary Disease

Dong

2018

Front. Immunol.

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Chronic obstructive pulmonary disease (COPD) is currently the third largest cause of human mortality in the world after stroke and heart disease. COPD is characterized by sustained inflammation of the airways, leading to destruction of lung tissue and declining pulmonary function. The main risk factor is known to be cigarette smoke currently. However, the strategies for prevention and treatment have not altered significantly for many years. A growing body of evidences indicates that the immune system plays a pivotal role in the pathogenesis of COPD. The repeated and progressive activation of immune cells is at least in part the source of this chronic inflammation. In this review paper, we have conducted an extensive literature search of the studies of immune cells in COPD patients. The objective is to assess the contributions of different immune cell types, the imbalance of pro/anti-inflammatory immune cells, such as M1/M2 macrophages, Tc1/Tc10, and Th17/Treg, and their mediators in the peripheral blood as well as in the lung to the pathogenesis of COPD. Therefore, understanding their roles in COPD development will help us find the potential target to modify this disease. This review focuses predominantly on data derived from human studies but will refer to animal studies where they help understand the disease in humans.

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Expression of Toll-like Receptor 2 and 4 in Peripheral Blood Neutrophil Cells from Patients with Chronic Obstructive Pulmonary Disease

Abstract: The increased expression of TLR2 and TLR4 suggests its role in disease pathogenesis of COPD. Smoke pack years was negatively associated with spirometric parameters in COPD patients. This may help to predict the smokers without COPD who risk developing the condition in the future.

Cited by 9 publications

References 35 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

<p>The Role of Toll-Like Receptors 2 and 4 in the Pathogenesis of Chronic Obstructive Pulmonary Disease</p>

Roles of Myeloid and Lymphoid Cells in the Pathogenesis of Chronic Obstructive Pulmonary Disease

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