Regulation of contact sensitivity in non‐obese diabetic (NOD) mice by innate immunity

Szczepanik, Marian; Majewska‐Szczepanik, Monika; Wong, F. Susan; Kowalczyk, Paulina; Pasare, Chandrashekhar; Li, Wen

doi:10.1111/cod.13046

Cited by 2 publications

(5 citation statements)

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“…It has been reported that B cells play a pathogenic role in the development of adipose tissue inflammation during obesity, causing increased plasma concentrations of IgG1 antibody 45,46 . The obese mice in our study have increased levels of TNP‐specific IgG1 antibody, the isotype associated with aggravated CHS to TNCB 47 . Several studies have indicated the role of IL‐17A in the onset and/or progression of chronic inflammatory diseases in obese mice and humans 48‐50 .…”

Section: Discussionsupporting

confidence: 55%

“…During inflammation, dDCs are mobilized rapidly from the skin and home to draining lymph nodes within 48 hours, preceding the arrival of LCs 54 . We have shown that the enhanced CHS response in TLR‐ and MyD88‐deficient NOD mice is associated with an enriched proportion of Th1‐inducing CD207 − CD103 + dDCs and a decreased proportion of tolerizing CD207 + CD103 − LCs in ALNs 47 . Our results in the current study showed that the increased CHS in obese mice was accompanied by reduced frequency of CD207 + CD103 − DCs, without affecting splenic Treg cells, although CD207 + dDCs or CD103 − dDCs can induce Treg cells in C57BL/6 mice 55‐57 .…”

Section: Discussionmentioning

confidence: 87%

“…45,46 The obese mice in our study have increased levels of TNP-specific IgG1 antibody, the isotype associated with aggravated CHS to TNCB. 47 Several studies have indicated the role of IL-17A in the onset and/or progression of chronic inflammatory diseases in obese mice and humans. [48][49][50] Our in vitro experiments revealed higher production of IL-17A by ELNCs F I G U R E 4 HFDIO promotes pro-inflammatory T cells and DCs in obese (group B) vs lean mice (group A) 4 days after TNCB sensitization.…”

Section: Discussionmentioning

confidence: 99%

“…54 We have shown that the enhanced CHS response in TLR-and MyD88-deficient NOD mice is associated with an enriched proportion of Th1-inducing CD207 À CD103 + dDCs and a decreased proportion of tolerizing CD207 + CD103 À LCs in ALNs. 47 Our results in the current study showed that the increased CHS in obese mice was accompanied by reduced frequency of CD207 + CD103 À DCs, without affecting splenic Treg cells, although CD207 + dDCs or CD103 À dDCs can induce Treg cells in C57BL/6 mice. [55][56][57] Nagao et al suggested that LCs and CD207 + dDCs act as negative regulators of Th1 cellular responses, since mice lacking both LCs and CD207 + dDCs have an increased number of CD4 + IFN-γ + SPLCs.…”

Section: Discussionmentioning

confidence: 99%

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Obesity aggravates contact hypersensitivity reaction in mice

et al. 2022

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Background Obesity is associated with chronic, low‐grade inflammation in tissues and predisposes to various complications, including inflammatory skin diseases. However, the link between obesity and contact hypersensitivity (CHS) is not fully understood. Objectives We sought to determine the influence of obesity on T helper 1 (Th1)–mediated CHS. Methods The activity/phenotype/cytokine profile of the immune cells was tested in vivo and in vitro. Using quantitative polymerase chain reaction (qPCR) and fecal microbiota transplantation (FMT), we tested the role of a high‐fat diet (HFD)–induced gut microbiota (GM) dysbiosis in increasing the effects of CHS. Results Exacerbated CHS correlates with an increased inflammation‐inducing GM in obese mice. We showed a proinflammatory milieu in the subcutaneous adipose tissue of obese mice, accompanied by proinflammatory CD4+ T cells and dendritic cells in skin draining lymph nodes and spleen. Obese interleukin (IL)‐17A−/−B6 mice are protected from CHS aggravation, suggesting the importance of IL‐17A in CHS aggravation in obesity. Conclusions Obesity creates a milieu that induces more potent CHS‐effector cells but does not have effects on already activated CHS‐effector cells. IL‐17A is essential for the pathogenesis of enhanced CHS during obesity. Our study provides novel knowledge about antigen‐specific responses in obesity, which may help with the improvement of existing treatment and/or in designing novel treatment for obesity‐associated skin disorders.

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Section: Discussionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Obesity aggravates contact hypersensitivity reaction in mice

et al. 2022

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“…Picryl chloride (PiCl), which has been utilized for a long time, is a simple chemical hapten reagent [19] used to prepare the delayed type hypersensitivity model animals [20,21]. Therefore, we used PiCl as the hapten to prepare the hypersensitivity model.…”

Section: Introductionmentioning

confidence: 99%

Exopolysaccharide Produced by Lactobacillus paracasei IJH-SONE68 Prevents and Improves the Picryl Chloride-Induced Contact Dermatitis

et al. 2019

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Allergic disease is one of the most important and common health problems worldwide. We have previously demonstrated that a fig leaf-derived lactic acid bacterium Lactobacillus (Lb.) paracasei IJH-SONE68 produces a novel exopolysaccharide (EPS). Furthermore, we have shown that the EPS inhibits the catalytic activity of hyaluronidase (EC 3.2.1.36) promoting inflammatory reactions. To evaluate the anti-allergy and anti-inflammatory effects of the EPS, in the present study, we employed the picryl-chloride-induced delayed-type (type IV) allergy model mice, which is used to evaluate the contact dermatitis. Oral administration of the EPS was observed to reduce the ear swelling in the model mice. We also observed that the overexpression of ear interleukin-4 (T helper (Th) 2 cytokine) mRNA and the increase in serum immunoglobulin E (IgE) are repressed. However, the expression of interferon-γ (Th1 cytokine) was not accelerated in all of the allergen-challenged model mice. The improvement may be responsible for the Th2 downregulation rather than the Th1 upregulation. In addition, the symptom of immediate-type (type I) allergy model mice was improved by oral administration of the IJH-SONE68 cell (data not shown). We can conclude that the IJH-SONE68-derived EPS is useful to improve the type I and IV allergies including atopic dermatitis.

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Regulation of contact sensitivity in non‐obese diabetic (NOD) mice by innate immunity

Abstract: Our results suggest that the autoimmune-prone NOD genetic background aggravates CHS regulated by innate immunity, through DCs and T effector cells.

Cited by 2 publications

References 44 publications

Obesity aggravates contact hypersensitivity reaction in mice

Obesity aggravates contact hypersensitivity reaction in mice

Exopolysaccharide Produced by Lactobacillus paracasei IJH-SONE68 Prevents and Improves the Picryl Chloride-Induced Contact Dermatitis

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