Toll-like Receptor 2 Down-regulation in Established Mouse Allergic Lungs Contributes to Decreased Mycoplasma Clearance

Wu, Qun; Martin, Richard J.; LaFasto, Spencer; Efaw, Benjamin; Rino, John G.; Harbeck, Ronald J.; Chu, Hong Wei

doi:10.1164/rccm.200709-1387oc

Cited by 70 publications

(69 citation statements)

References 50 publications

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“…More recently, atypical infection has been associated with more severe asthma exacerbations, as shown by spirometry and symptom severity scores [56]. In support of the hypothesis that asthmatic airways are more susceptible to M. pneumoniae infection, Toll-like receptor 2 expression and interleukin (IL)-6 production are downregulated by M. pneumoniae infection during ongoing ovalbumin-induced allergic inflammation [57]. Moreover, airway epithelial cells from asthmatic subjects show increased production of mucin 5 subtypes A and C (the major airway mucin) when infected with M. pneumoniae compared to normal controls [58].…”

Section: Infection Among Factors Precipitating Asthma Exacerbationsmentioning

confidence: 92%

Childhood asthma and infection: virus-induced exacerbations as determinants and modifiers: Figure 1–

Xepapadaki¹,

Papadopoulos²

2010

Eur Respir J

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Respiratory infections have been implicated in the origin and exacerbation of asthma in a variety of ways; however, systemisation of this knowledge in a way helpful for disease management remains suboptimal.Several conceptual issues need to be taken into account: the fact that the effects of an infection may vary according to genetic background, the current immune status of the host, and parallel environmental stimuli, in addition to the particular infectious agent itself. Moreover, childhood is a very special period because of the continuous processes taking place, such as neural, immune and respiratory maturation.Epidemiological studies have convincingly demonstrated that the majority of asthma exacerbations, in both adults and children, follow viral upper respiratory tract infections. Asthma exacerbations are still often unresponsive to current asthma treatment, and new therapeutic approaches are required.This review presents current knowledge on the associations between infection and exacerbation of established asthma with respect to definitions, epidemiology, mechanisms and treatment.

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Section: Infection Among Factors Precipitating Asthma Exacerbationsmentioning

confidence: 92%

Childhood asthma and infection: virus-induced exacerbations as determinants and modifiers: Figure 1–

Xepapadaki¹,

Papadopoulos²

2010

Eur Respir J

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“…It was observed by some authors that lipoprotein triacylglycerol originated from MP activate NF-κB through TLR1 and TLR2 but not TLR6 [17,41]. However, the interruption of TLR2 signaling that was induced by MP infection by the release of IL-4 and IL-13 (allergic cytokines) decreased the clearance of MP from the lungs of mice, leaving the tissue more susceptible to bacterial diseases [42]. Using ISH, we observed correlations between Cp and TLR2 in the aneurysm group.…”

Section: Discussionmentioning

confidence: 64%

Involvement of TLR2 and TLR4, <i>Chlamydophila pneumoniae</i> and <i>Mycoplasma pneumoniae</i> in adventitial inflammation of aortic atherosclerotic aneurysm

Assis¹,

Higuchi²,

Reis³

et al. 2014

WJCD

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Aortic atherosclerotic aneurysm (AAA) is associated with adventitial inflammation where infection is suggested to have a role. Co-infection withChlamydophila pneumoniae (Cp) and Mycoplasma pneumoniae (Mp) was linked with coronary plaque rupture, in association with vessel dilatation and adventitial inflammation. Pathogens are recognized by Toll-like receptors (TLRs) development of the inflammatory process. Objective: Here, we studied whether co-infection by Cp and Mp was involved in the increased inflammation present in AAA and if it could be associated with deficient expression of TLRs. We compared human samples of AAA with non-dilated human aortic atherosclerotic lesions, regarding the amount of Cp and Mp antigens, and expression of TLR2 and TLR4. Methods: Two groups of aorta fragments were analyzed: G1 (n = 13) moderate atherosclerosis and G2 (n = 14) AAA samples, through immunohistochemistry and in situ hybridization methods. Results: Mp and Cp antigens in intima/medial layer were greater in G2 than G1, with no difference in adventitia. TLR2 and TLR4 were higher in G2 than G1 adventitia fat. There was a correlation between Mp versus TLR2 and of TLR4 in intima/medial layer and in adventitia of G1, but there was a lack of correlation in G2. In Cp adventitia, the correlation in G1 was high with TLR2 but not with TLR4, and in G2 the correlation was positive for both TLRs. Conclusion: This study favors the concept that symbiotic co-infection by Cp and Mp participates in the pathogenesis of AAA. It also emphasizes that adventitial fat is the initial site for colonization of these bacteria that probably reach the tissue through vasa vasorum. An exacerbated immune reaction is not efficient to control the infection that reaches and proliferates in high levels at the medial and intimal layer, contributing to the development of vessel dilatation.

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“…Delayed postnatal maturation of the immune system, including a delayed transition from Th2 to Th1 bias, is a risk factor for respiratory infections [30]. In a mouse model, after infection of the lungs with Chlamydia muridarum, IL-13, a Th2 cytokine, is rapidly produced and promotes susceptibility to infection, possibly related to impairment of macrophage phagocytic function [31]. Downregulation of TLRs may be responsible for increased susceptibility of asthmatics to mycoplasma infection, as mycoplasma clearance in an allergic mouse model has been demonstrated to be due to TLR2 down-regulation [32].…”

Section: Discussionmentioning

confidence: 99%

Alzheimer’s Disease of the Immune System: A New Variant of Immune Deficiency

Melamed¹

2016

Immunother Open Acc

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The interaction between infectious pathogens and the immune system has been a focus of research for many years. However, the failure of re-recognition or immune memory of infectious pathogen remains a clear mystery A memory B cell defect coupled with low levels of C1-INH and/or C1-INH function-failure of both the innate and adaptive immune components-may lead to persistent unresolved infection. Here we present 3 case studies that explore the abnormal immune response that may lead to persistent infection. These cases offer possible clarification of a longstanding clinical observation that some patients may develop a post infectious syndrome that includes various neurological symptoms and unusual fatigue. These patients may have positive serology seen only during acute infectious phase and have a documented positive PCR, suggesting active presence of the pathogen. The unusual presentation is prolonged and irreversible. We use the term "Alzheimer's disease of the immune system" to identify this subtype due to the memory defect of the immune system. As we identified 3 common immune defects in all cases, we suggest a new immune deficiency leading to the post infectious syndrome.

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Toll-like Receptor 2 Down-regulation in Established Mouse Allergic Lungs Contributes to Decreased Mycoplasma Clearance

Cited by 70 publications

References 50 publications

Childhood asthma and infection: virus-induced exacerbations as determinants and modifiers: Figure 1–

Childhood asthma and infection: virus-induced exacerbations as determinants and modifiers: Figure 1–

Involvement of TLR2 and TLR4, <i>Chlamydophila pneumoniae</i> and <i>Mycoplasma pneumoniae</i> in adventitial inflammation of aortic atherosclerotic aneurysm

Alzheimer’s Disease of the Immune System: A New Variant of Immune Deficiency

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Toll-like Receptor 2 Down-regulation in Established Mouse Allergic Lungs Contributes to Decreased Mycoplasma Clearance

Cited by 70 publications

References 50 publications

Childhood asthma and infection: virus-induced exacerbations as determinants and modifiers: Figure 1–

Childhood asthma and infection: virus-induced exacerbations as determinants and modifiers: Figure 1–

Involvement of TLR2 and TLR4, &lt;i&gt;Chlamydophila pneumoniae&lt;/i&gt; and &lt;i&gt;Mycoplasma pneumoniae&lt;/i&gt; in adventitial inflammation of aortic atherosclerotic aneurysm

Alzheimer’s Disease of the Immune System: A New Variant of Immune Deficiency

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Product

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Involvement of TLR2 and TLR4, <i>Chlamydophila pneumoniae</i> and <i>Mycoplasma pneumoniae</i> in adventitial inflammation of aortic atherosclerotic aneurysm