Inverse association between endotoxin exposure and canine atopic dermatitis

Beeck, F.A. Looringh van; Hoekstra, Hilde; Brunekreef, Bert; Willemse, Ton

doi:10.1016/j.tvjl.2010.10.027

Cited by 16 publications

(15 citation statements)

References 32 publications

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“…The reason for this decrease is uncertain, although the authors state that they were unable to relate the decrease to bathing frequency (F. A. Looringh van Beeck, 2011, unpublished data). In the same study, no significant association was seen between atopic status and the levels of exposure to fungal glucans in the hair coat and environment (floor, bedding) or to environmental endotoxin levels …”

Section: Environmental Contributions To Atopic Dermatitismentioning

confidence: 83%

“…In contrast to the human literature, there are very few reports specifically investigating the role of environmental microbial components in the development or clinical course of canine AD. One study demonstrated a significant inverse association between canine hair coat endotoxin levels and atopic status, although this effect was no longer significant once the values were adjusted for age and sex . The reason for this decrease is uncertain, although the authors state that they were unable to relate the decrease to bathing frequency (F. A. Looringh van Beeck, 2011, unpublished data).…”

Section: Environmental Contributions To Atopic Dermatitismentioning

confidence: 99%

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Review: Role of genetics and the environment in the pathogenesis of canine atopic dermatitis

Bizikova

Pucheu‐Haston

Eisenschenk³

et al. 2015

Veterinary Dermatology

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It is becoming clear that canine AD is genotypically complex and influenced by a variety of environmental factors. Well-designed studies with sufficient statistical power will be critical to identify the complex genetic and environmental factors involved in disease development and progression. Recognition of such factors may help to identify new targets for therapy and enable better disease prevention and management.

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Section: Environmental Contributions To Atopic Dermatitismentioning

confidence: 83%

Section: Environmental Contributions To Atopic Dermatitismentioning

confidence: 99%

Review: Role of genetics and the environment in the pathogenesis of canine atopic dermatitis

Bizikova

Pucheu‐Haston

Eisenschenk³

et al. 2015

Veterinary Dermatology

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“…However, accumulating evidence suggests that endotoxin exposure is inversely associated with developing atopy, but positively associated with an increased risk of asthma and asthma severity in both adults and children 56. Similarly, increasing evidence suggests that the infectious burden in early childhood is positively associated with the development of atopic asthma 57,58.…”

Section: Endotoxin Exposure As a Risk Factor For Allergic Asthmamentioning

confidence: 99%

Immunopathogenesis of Allergic Asthma: More Than the Th2 Hypothesis

Kim

Jeon

2013

Allergy Asthma Immunol Res

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Asthma is a chronic obstructive airway disease that involves inflammation of the respiratory tract. Biological contaminants in indoor air can induce innate and adaptive immune responses and inflammation, resulting in asthma pathology. Epidemiologic surveys indicate that the prevalence of asthma is higher in developed countries than in developing countries. The prevalence of asthma in Korea has increased during the last several decades. This increase may be related to changes in housing styles, which result in increased levels of indoor biological contaminants, such as house dust mite-derived allergens and bacterial products such as endotoxin. Different types of inflammation are observed in those suffering from mild-to-moderate asthma compared to those experiencing severe asthma, involving markedly different patterns of inflammatory cells and mediators. As described in this review, these inflammatory profiles are largely determined by the involvement of different T helper cell subsets, which orchestrate the recruitment and activation of inflammatory cells. It is becoming clear that T helper cells other than Th2 cells are involved in the pathogenesis of asthma; specifically, both Th1 and Th17 cells are crucial for the development of neutrophilic inflammation in the airways, which is related to corticosteroid resistance. Development of therapeutics that suppress these immune and inflammatory cells may provide useful asthma treatments in the future.

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“…So far, the effect of different TLR4 antagonists on the AD development is ambiguous. A case‐control study showed that LPS exposure is inversely associated with AD . It has been demonstrated that skin‐expressed HSPs could activate TLR4 in DCs, which then initiated T cell‐mediated immune responses in allergic contact hypersensitivity .…”

Section: Discussionmentioning

confidence: 99%

“…A case-control study showed that LPS exposure is inversely associated with AD. [43] It has been demonstrated that skin-expressed HSPs could activate TLR4 in DCs, which then initiated T cell-mediated immune responses in allergic contact hypersensitivity. [44] By contrast, systemic HMGB1 administration ameliorated the skin inflammatory changes in the mouse model of allergic contact dermatitis.…”

Section: Discussionmentioning

confidence: 99%

Toll‐like receptor 4 attenuates a murine model of atopic dermatitis through inhibition of langerin‐positive DCs migration

Lin

Xie

Chen

et al. 2018

Experimental Dermatology

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Atopic dermatitis (AD) is a common chronic inflammatory skin disease that is often associated with skin barrier dysfunction leading to a higher frequency of bacterial and viral skin infections. Toll-like receptor (TLR) 4 on resident skin cells was involved in sensing pathogens and eliciting pathogen-specific innate and adaptive immune responses. Previous studies have demonstrated that TLR4 was linked to AD severity in context of pathogen infection. However, the immune regulatory role of TLR4 in AD remains to be defined. We here investigated the immune regulatory function of TLR4 in AD induced by repeated epicutaneous application of a hapten, 2,4-dinitrochlorobenzene (DNCB). Our results showed that TLR4-deficient (TLR4 ) mice exhibited more severe AD symptoms than WT mice after DNCB challenge. The DNCB-treated TLR4 mice also displayed higher expression levels of inflammatory cytokines and stronger Th2 response than WT counterparts. Moreover, the skin expression of thymic stromal lymphopoietin (TSLP), an important potential contributor to allergic inflammation, was significantly elevated in TLR4 mice compared with that in WT mice upon DNCB administration. Furthermore, we demonstrated that the migration of langerin-positive dendritic cells (DCs) into draining lymph nodes was enhanced in TLR4 mice following DNCB challenge, which is partially dependent on the production of pro-inflammatory cytokine TNF-α. Together, these results determined that TLR4 affected the hapten-induced skin inflammation in the absence of exogenous pathogen infection, suggesting that TLR4 not only regulates infection but also may serve as a modulator of the immune response during AD development.

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Inverse association between endotoxin exposure and canine atopic dermatitis

Cited by 16 publications

References 32 publications

Review: Role of genetics and the environment in the pathogenesis of canine atopic dermatitis

Review: Role of genetics and the environment in the pathogenesis of canine atopic dermatitis

Immunopathogenesis of Allergic Asthma: More Than the Th2 Hypothesis

Toll‐like receptor 4 attenuates a murine model of atopic dermatitis through inhibition of langerin‐positive DCs migration

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